dialisis peritoneal

II. NKF-K/DOQI CLINICAL PRACTICE GUIDELINES FORPERITONEAL DIALYSIS ADEQUACY:

UPDATE 2000

NOTE: The citation for these guidelines should read as follows: National Kidney Foundation. K/DOQIClinical Practice Guidelines for Peritoneal Dialysis Adequacy, 2000. Am J Kidney Dis 37:S65-S136,2001 (suppl 1)

S65

Acronyms and Abbreviations

Abbreviation TermACE angiotensin-converting enzymeBSA body surface areaBUN blood urea nitrogen concentrationCANUSA Canada/USA Peritoneal Dialysis StudyCAPD continuous ambulatory peritoneal dialysisCCPD continuous cycling peritoneal dialysisCCr creatinine clearanceCr Cr residual renal creatinine clearanceCKD chronic kidney diseaseDI dialysis indexDPI dietary protein intakeeC effective clearanceESRD end-stage renal diseaseGFR glomerular filtration rateHD hemodialysisKp Cr peritoneal creatinine clearanceKpt/Vurea the peritoneal component of Kt/Vurea

Kprt/Vurea the sum of peritoneal and renal Kt/Vurea. These terms are interchangeable in that Kt/Vurea is total unless otherwise noted.

Kt/Vurea urea clearance � time normalized by total body water, the volume ofdistribution of urea

Krt/Vurea the renal component of Kt/Vurea

MTC mass transfer coefficientn normalizednBSA normalized body surface areaNIPD nocturnal intermittent peritoneal dialysisnPCR normalized protein catabolic ratenPNA normalized protein equivalent of total nitrogen appearancenV normalized volumePCR protein catabolic ratePD peritoneal dialysisPET peritoneal equilibration testPNA protein equivalent of nitrogen appearanceQOL quality of lifeRKF residual kidney functionRRF residual renal functionSGA subjective global assessmentSHR standardized hospitalization ratesSUN serum urea nitrogen concentrationt timeUKM urea kinetic modelingUNA urea nitrogen appearanceURR urea reduction ratioUSRDS United States Renal Data SystemV volume of distribution. When referring to urea, this is total body water

S66

Introduction

T HIS WORK GROUP was charged with pre-paring practice guidelines for the “ad-

equacy of peritoneal dialysis,” a topic that couldbe defined broadly or narrowly. The Work Groupelected to focus its guidelines on those areas of“adequacy” that needed the most urgent develop-ment, knowing that subsequent guidelines willbe developed or that others were currently underdevelopment (eg, for management of peritoni-tis). In addition, the Work Group focused ontopics for which guidelines would likely have thegreatest impact on patient outcomes. However,the Work Group’s focus should not be construedto mean that areas not covered are unimportant.

Some external reviewers criticized these guide-lines as too complex, while others wrote thatthey were not thorough enough. Some wantedguidelines merged, and others thought the guide-lines were too dense. The Work Group consid-ered all these issues.

We advise the reader to first become familiarwith the Table of Contents, which provides alisting of the Clinical Practice Guidelines forPeritoneal Dialysis Adequacy; detailed ration-ales are provided for each guideline. Redundan-cies are often intentional because it is anticipatedthat a reader might review only selected topics.However, the Work Group considers these guide-lines as best viewed in their entirety, rather thanin their component parts.

There is a paucity of data on children in theareas covered by these guidelines. Pediatricianswere represented on the Work Group, and out-side pediatric consultations were obtained. Be-cause some recommendations for adults do notapply to children, additional recommendationsare included when appropriate for pediatric pa-tients. For the purpose of these guidelines, achild was considered to be a patient less than 19years of age.

An “effective dose” is that which achieves its

stated goal. That goal is some form of outcomemeasure(s), and could be determined by patient,provider, payer, regulator or a combination ofthese parties. At the lower extreme is the “mini-mal effective dose.” In certain circumstances thismay be interpreted as “adequate.” At the otherextreme is the “maximal effective dose,” thedose above which there are no additional ben-efits. For hemodialysis and peritoneal dialysisthe maximal effective dose is not known. Some-where between these extremes is the “optimaldose,” the dose above which the additional de-rived benefit does not justify the additional costor burden. If one accepts this definition, theWork Group intended to more precisely define“optimal dose” targets in a clinically relevantand quantitative fashion. It was the intention ofthe Work Group to bring “adequate dose” to thelevel of “optimal dose” by raising the outcomegoals or expectations. The present guidelinesattempt to make recommendations based on avail-able scientific/medical evidence, resorting to ex-pert opinion only when necessary. It is clearlystated in each guideline title when recommenda-tions were based on evidence, opinion, or both.Even when guidelines were based on opinion,that opinion is supported by direct or extrapo-lated evidence.

These guidelines are intended for use by healthcare professionals trained to understand varia-tions in the practice of medicine and the neces-sity for such variation. These guidelines are notintended for punitive use by any oversight offi-cial who does not understand the reasons or thenecessity for practice variations including varia-tions in societies different from that of the UnitedStates.

© 2001 by the National Kidney Foundation, Inc.0272-6386/01/3701-0103$3.00/0doi:10.1053/ajkd.2001.20778

American Journal of Kidney Diseases, Vol 37, No 1, Suppl 1 (January), 2001: pp S67 S67

I. Initiation of Dialysis

BACKGROUND

Two clinical guidelines for when to initiatedialysis are provided because there appear to betwo independent predictors of clinical outcome.The first guideline is based on the level of kidneyfunction (as measured by Krt/Vurea per week); thesecond is based on nutritional indices and islocated in the K/DOQI Clinical Practice Guide-lines in Chronic Renal Failure (Guideline 27).2

Although less than 1% of American dialysispatients begin dialysis with a serum creatinineconcentration �8.0 mg/dL or a CCr �10 mL/min, approximately 60% suffer from nausea/vomiting at the time of dialysis initiation.3 Thus,the likelihood of malnutrition in this populationis high. Evidence from the Modification of Dietin Renal Disease (MDRD) study4 and a recentlarge Australian study5 clearly show that whenthe glomerular filtration rate (GFR) decreases to25 to 50 mL/min, patients adapt by reducingtheir protein intake. Protein intake continues todecline as kidney disease progresses to kidneyfailure, administratively termed end-stage renaldisease (ESRD). These observations have beencorroborated in a prospective study.6 As kidneyfunction deteriorates, protein and energy intakedecreases, leading to changes in body weight, fatmass, serum albumin, and transferrin concentra-tions. Earlier initiation of dialysis may prevent orperhaps even reverse this deterioration in nutri-tional status. Increased serum albumin concentra-tion has been shown to parallel the increase inKt/Vurea for HD patients.7 In addition, an edito-rial review of cited data8 suggests that albuminlevel at initiation of dialysis is predictive ofsurvival.9

Adverse clinical and economic consequencesof failure to properly manage patients with pro-gressive chronic kidney disease as they approachESRD and become dialysis dependent were firstdescribed in Britain.10 These observations havenow been corroborated in other regions of Brit-ain, the United States, and France.11-14 Specifi-cally, costs, hospitalization, and morbidities de-crease if attention is paid to nutrition, acid-basestatus, hypocalcemia, hyperphosphatemia, ane-mia, hypertension, volume status, and dialysisaccess (vascular or peritoneal). Hence, it is likelythat delays in referral for initiation of dialysis

result in unnecessary morbidity and potentiallyhigher costs as well. While seeing a nephrologistdoes not guarantee that patients will be ad-equately prepared and referred for dialysis, itdramatically increases the likelihood that thiswill occur.13

The initiation of dialysis guidelines as de-scribed in this section are based on adult data. Nosuch data exist yet in children.

GUIDELINE 1

When to Initiate Dialysis—Kt/V urea Criterion(Opinion)

Unless certain conditions are met, patientsshould be advised to initiate some form of dialy-sis when the weekly renal Kt/Vurea (Krt/Vurea)falls below 2.0. The conditions that may indicatedialysis is not yet necessary even though theweekly Krt/Vurea is less than 2.0 are:

1. Stable or increased edema-free body weight.Supportive objective parameters for adequatenutrition include a lean body mass �63%, subjec-tive global assessment score indicative of ad-equate nutrition (see Guideline 12: NutritionalStatus Assessment, and Appendix B: DetailedRationale for Guideline 2) and a serum albuminconcentration in excess of the lower limit for thelab, and stable or rising; and

2. Nutritional indications for the initiation ofrenal replacement therapy are detailed in Guide-line 27 of the NKF-K/DOQI Clinical PracticeGuidelines on Nutrition, part of which is repro-duced as Guideline 2 of the PD Adequacy Guide-lines.

3. Complete absence of clinical signs or symp-toms attributable to uremia.

A weekly Krt/Vurea of 2.0 approximates a kid-ney urea clearance of 7 mL/min and a kidneycreatinine clearance that varies between 9 to 14mL/min/1.73 m2. Urea clearance should be nor-malized to total body water (V) and creatinineclearance should be expressed per 1.73 m2 ofbody surface area. The GFR, which is estimatedby the arithmetic mean of the urea and creatinineclearances, will be approximately 10.5 mL/min/1.73 m2 when the Krt/Vurea is about 2.0.

Rationale A detailed rationale is described inAppendix A. The following is a summary.

It is paradoxical that nephrologists have fo-

American Journal of Kidney Diseases, Vol 37, No 1, Suppl 1 (January), 2001: pp S68-S71S68

cused on optimizing urea clearance once patientsare started on dialysis, but have accepted muchlower levels of kidney urea clearance during thepre-dialysis phase of patient management. Forexample, a weekly total (residual renal plus peri-toneal dialysis) Kt/Vurea (Kprt/Vurea) of 2.0 orhigher is associated with improved outcomes inpatients on PD (see Guideline 15: Weekly Doseof CAPD), yet dialysis is usually not initiateduntil weekly Krt/Vurea falls to the range of 0.71 to1.3. There is no definitive direct proof for thebelief that a given level of urea clearance by thekidney is associated with better control of uremiathan PD with this same urea clearance. In fact,recent studies suggest that the relationship be-tween protein intake and weekly Kt/Vurea is nearlyidentical in patients with chronic renal failure notyet on dialysis and in patients on PD. Thus, untilproven otherwise, residual kidney and peritonealclearances of small solutes should be consideredequivalent.

Once Krt/Vurea falls below 2.0 per week, pa-tients should be considered at increased risk formalnutrition and uremic complications. With fur-ther decreases in Krt/Vurea in the absence of renalreplacement therapy, the risk increases. Dialysis,or some form of renal replacement therapy, shouldbe strongly considered when Krt/Vurea falls be-low 2.0 (or CCr falls in the range of 9 to 14mL/min/1.73 m2) and definitely implemented if:

1. Despite vigorous attempts to optimize pro-tein and energy intake, any of the followingnutritional indicators show evidence of deteriora-tion: (a) more than a 6% involuntary reduction inedema-free usual body weight (%UBW) or toless than 90% of standard body weight (NHANESII) in less than 6 months; (b) a reduction in serumalbumin by greater than or equal to 0.3 g/dL andto less than 4.0 g/dL (see Nutrition Guideline 3),in the absence of acute infection or inflamma-tion, confirmed by repeat laboratory testing; or(c) a deterioration in SGA by one category (ie,normal, mild moderate, severe; see NutritionGuideline 9 and Nutrition Appendix VI).

If PD is initiated, the Kpt/Vurea could be in-creased incrementally so the combined weeklyvalue of Krt/Vurea � Kpt/Vurea (Kprt/Vurea or totalKt/Vurea) does not fall below the target level of2.0. With the incremental initiation approachfrequent measurement of residual kidney func-

tion (RKF) will be necessary to assure that totaldelivered solute removal does not drop belowtargets (see Guidelines 3: Frequency of Deliv-ered PD Dose and Total Solute Clearance Mea-surement Within Six Months of Initiation, andGuideline 5: Frequency of Measurement of Kt/Vurea, Total CCr, PNA, and Total Creatinine Ap-pearance). Alternatively, the initiation of a “fulldose” of PD may be offered (equivalent of four2-L exchanges per day, which may yield a weeklyKpt/Vurea of 1.5 to 2.0, depending on transportcharacteristics, ultrafiltration, and body size).With initiation of “full dose” PD, frequency ofmeasurement of RRF can be less intense.

The Work Group strongly supports the opin-ion that the PD outcome data for a weeklyKt/Vurea of �2.0 are so compelling that using thesame figure for initiation of dialysis justifies thesmall risks of performing peritoneal dialysis.Those risks include infections and the possibilitythat increasing the length of time on PD contrib-utes to eventual patient “burn-out.” If a patient issuspected to be at high risk for these complica-tions, PD may not be the best choice for renalreplacement therapy. The Work Group acknowl-edges that the risks of early initiation of PD arenot clearly known, but that the risks of lateinitiation are known and are unacceptable. Fur-thermore, not knowing which initiation strategy(incremental versus full therapy initiation) isbetter, the Work Group recommends that eitherapproach be used to reach or exceed targets.

Compared to CAPD, it is more complex tocalculate the incremental dose of hemodialysis(HD) that would be needed such that the totalcontinuous delivered weekly Kt/Vurea would begreater than 2.0. However, it can be estimatedusing the fundamental assumption underlyingCAPD, that at the same protein catabolic rate,continuous renal replacement therapy must keepthe steady state BUN equal to the average pre-hemodialysis BUN. (See Appendix G for furtherdiscussion of this assumption.) If weekly Krt/Vurea is 1.6 , for example, a one time per weekHD treatment must deliver an equilibrated(double-pool) Kt/Vurea of 2.0 to achieve a totalcontinuous weekly Kt/Vurea equivalent to 2.0.This is quite difficult to achieve, so two HDtreatments per week may be more realistic forthis level of RRF. If weekly Krt/Vurea is 0.5, two

INITIATION OF DIALYSIS S69

HD treatments must each deliver an equilibrated(double-pool) Kt/Vurea of 2.0 to achieve a totalcontinuous weekly Kt/Vurea equivalent to 2.0.This is also quite difficult to achieve, so threeHD treatments per week may be more realisticfor this level of RKF. More technical detailsabout intermittent HD are described in AppendixA, including the role of biocompatible mem-branes to help preserve RKF.

It is a general consensus that patients withdiabetes should initiate dialysis at levels of RKFhigher than in patients with causes of ESRDother than diabetes. That practice is not alteredby this guideline.

The Work Group also recognizes that for manyclinicians, initiating dialysis based on Kt/Vurea isa new concept. Therefore, we have attempted toequate this to the traditional measure of ureaclearance, CCr, and GFR (estimated by the arith-metic mean of urea and creatinine clearance).

The Work Group recognizes that the patientwill play a major role in accepting the initiationof dialysis based on a certain “laboratory value.”It is the responsibility of the care providers tomake clear to the patient the rationale for initiat-ing dialysis when the above conditions becomeapplicable. In particular, the nephrologist mustexplain to the patient the risk of malnutritionwith delayed initiation of dialysis and the stronginferential evidence that survival might be im-proved with an earlier start of dialysis. Thus,appropriate patient education regarding an in-formed decision about dialysis is necessary. Medi-cal conditions that may explain why dialysis isnot being initiated when weekly Krt/Vurea is lessthan 2.0 need to be documented. These condi-tions are described above.

Some individuals have expressed concern thatthis guideline will run afoul of the Health CareFinancing Administration (HCFA) regulationsregarding the initiation of dialysis (eg, form2728, ESRD Medicare Medical Evidence Re-port). The leadership of the NKF-K/DOQI isworking with HCFA to ensure that this will notbe the case.

GUIDELINE 2

Indications for Renal Replacement Therapy

In patients with chronic kidney failure (eg,GFR � 15 to 20 mL/min) who are not undergo-

ing maintenance dialysis, if protein-energy mal-nutrition (PEM) develops or persists despite vig-orous attempts to optimize protein and energyintake and there is no apparent cause for malnu-trition other than low nutrient intake, initiation ofmaintenance dialysis or a renal transplant isrecommended. (Opinion)

Note: This is Guideline 27 of the K/DOQINutrition Guidelines, reproduced here withoutthe specific reference citations included. See theNutrition Guidelines2 for these details. ThisGuideline was written by members of both thePD Adequacy and Nutrition Work Groups.

Rationale It is well documented that mortal-ity and morbidity are increased in individualswith ESRD who begin dialysis therapy withovert evidence of PEM. Accumulating evidencealso indicates that initiation of dialysis more inline with current NKF-K/DOQI practice guide-lines (ie, GFR �10.5 mL/min) results in im-proved patient outcomes compared with whendialysis is delayed until the GFR is �5 mL/minand symptomatic uremia and associated medicalcomplications are present. Furthermore, there isevidence that initiating maintenance dialysis un-der these circumstances, and when there hasbeen nutritional deterioration, results in an im-provement in nutritional indices. There is noevidence that earlier initiation of dialysis leads toimproved nutritional status among patients with-out overt uremia. Moreover, it has not beenestablished that improved nutritional status at theinitiation of dialysis directly leads to improvedsurvival or fewer dialysis-related complications.Despite the lack of evidence from controlledclinical trials, interventions that maintain or im-prove nutritional status before the requirementfor renal replacement therapy are likely to resultin improved long-term survival.

There is ample evidence that the survival ofpatients with ESRD is closely associated withtheir nutritional status (Guidelines 3 through 6,8, 18, and 23). These findings have been demon-strated not only in large, diverse populations ofprevalent maintenance dialysis (MD) patients,but also in patients commencing MD therapy.Hypertension, pre-existing cardiac disease, andlow serum albumin concentrations were indepen-dently associated with diminished long-term sur-vival in 683 ESRD patients who started dialysis

GUIDELINES FOR PERITONEAL DIALYSIS ADEQUACYS70

during 1970 through 1989. In 1,982 hemodialy-sis (HD) patients, a low serum albumin concen-tration at the initiation of dialysis was associatedwith a significant increase in the relative risk ofdeath. A direct relation between serum albuminand survival and an independent association be-tween modified SGA and survival was observedin 680 incident CPD patients. In contrast, in onestudy no significant associations were found be-tween serum albumin, creatinine, and urea con-centrations and survival in incident HD patients.The sample size in the latter study was relativelysmall (n � 139), and 94% of the study samplewere black (83%) or Hispanic (11%). No studieshave specifically examined the relations amongother nutritional indicators (eg, %SBW, PNA,and DEXA) and survival in incident HD or peri-toneal dialysis patients.

Low-protein (eg, 0.60 g protein/kg/d), highenergy (35 kcal/kg/d) diets may retard the rate ofprogression of chronic kidney disease (CKD)and should maintain patients with chronic renaldisease in good nutritional status (Guidelines 24and 25). However, it is recognized that suchlow-protein diets may not maintain adequatenutritional status in all patients, particularly if anadequate energy intake is not maintained (Guide-line 25). Furthermore, there is evidence that thespontaneous intake of protein and energy, andother indicators of nutritional status, tend todiminish in patients with progressive CKD whoare consuming unregulated diets. Therefore, pa-tients with CKD need to undergo nutritionalassessment at frequent intervals so that any dete-rioration in nutritional status can be detectedearly (Guidelines 23 and 26 and Appendix IV).The plan of care and nutritional interventionsoutlined in Guideline 18 for the nutritional man-agement of the dialysis patient is also appropri-ate for patients with progressive CRI.

Because of the association between PEM and

poor outcome, it is recommended that MD beinitiated or kidney transplantation performed inpatients with advanced CKD (ie, GFR �20 mL/min) if there is evidence of deteriorating nutri-tional status or frank PEM, no other apparentcause for the malnutrition, and efforts to correctthe nutritional deterioration or PEM are unsuc-cessful, despite the absence of other traditionalindications for dialysis (eg, pericarditis or hyper-kalemia). Although the following criteria are notconsidered rigid or definitive, initiation of renalreplacement therapy should be considered if,despite vigorous attempts to optimize proteinand energy intake, any of the following nutri-tional indicators show evidence of deterioration:(1) more than a 6% involuntary reduction inedema-free usual body weight (%UBW) or toless than 90% of standard body weight (NHANESII) in less than 6 months; (2) a reduction in serumalbumin by greater than or equal to 0.3 g/dL andto less than 4.0 g/dL (Guideline 3), in the absenceof acute infection or inflammation, confirmed byrepeat laboratory testing; or (3) a deterioration inSGA by one category (ie, normal, mild, moder-ate, or severe; Guideline 9 and Appendix VI).

RECOMMENDATIONS FOR RESEARCH

1. Studies to assess the optimal timing andindications for commencing renal replacementtherapy are needed.

2. Serial evaluations of nutritional status in thecourse of these studies will help to determinewhether initiation of dialysis indeed improvesnutritional status.

3. Studies should be conducted to determinewhether any GFR level can be used to indicatewhen maintenance dialysis should be initiated.

4. Whether earlier initiation of renal replace-ment therapy can prevent the development orworsening of PEM and its attendant complica-tions needs to be evaluated in a controlled study.

INITIATION OF DIALYSIS S71

II. Measures of Peritoneal Dialysis Dose

GUIDELINE 3

Frequency of Delivered PD Dose and TotalSolute Clearance Measurement Within SixMonths of Initiation (Opinion)

The total solute clearance (delivered PD doseplus residual kidney function) should be mea-sured at least twice and possibly three timeswithin the first 6 months after initiation of PD.For patients initiating dialysis for the first timeand/or patients with substantial residual kidneyfunction, the first measurement should be per-formed approximately 2 to 4 weeks after initia-tion of PD. For patients transferring from anotherrenal replacement therapy to PD and/or for pa-tients who do not have substantial residual kid-ney function, the first measurement of delivereddose of PD should be made by 2 weeks afterinitiation of PD. To establish a baseline, at leastone and possibly two additional measurementswill need to be performed in the subsequent 5months. The frequency of measurement of re-sidual kidney function depends on the PD pre-scription of incremental versus full dose (seeTable II-1).

Rationale Adequate total solute clearance (de-livered dose of PD plus residual kidney function)

will improve patient outcomes (see Guideline15: Weekly Dose of CAPD). To assure deliveryof adequate solute clearance, measurements forsolute clearance are required. In dialysis, as inother human endeavors, continuous educationand repetition of a process diminish the fre-quency of errors, or at least increase the likeli-hood of recognition of such errors and compensa-tion for them. Furthermore, physiologicalvariations occur which must be taken into ac-count.17 These lines of reasoning apply to mea-surement of the dose of PD. Thus, measurementof delivered PD dose should be repeated periodi-cally. The recommendation to measure CCr andKt/Vurea three times within the first 6 monthsrelates to items discussed in Guideline 7: PDDose Troubleshooting, specifically, establishinga baseline creatinine excretion and followingresidual kidney function. The rationale for threemeasurements in the first 6 months is to establisha more accurate baseline excretion of creatinine.

Two measurements within the first 6 monthsare probably sufficient if the results are similar.Based on our collective personal experience, theWork Group believes that patient compliancewith a prescribed PD regimen is highest soonafter initiation of PD, eg, within the first 6months; hence, this period is used to establish abaseline.

Delivered peritoneal dialysis dose depends onmany factors, including the transport propertiesof the peritoneal membrane, assessed by theperitoneal equilibration test (PET).18,19 There isevidence that the PET performed within the firstweek after initiation of PD may yield highertransport results than a PET performed a fewweeks later.20 This difference is statistically sig-nificant, but may not be clinically relevant. Itmay be more convenient to perform the first PETat the end of training, rather than at the end of thefirst month, and the Work Group thinks this isacceptable. However, the results after a month ofPD may more accurately reflect peritoneal trans-port properties for the subsequent period.

In patients initiating ESRD therapy for thefirst time who have some RKF, delaying the PETand the first measurement of delivered dose for amonth is safe and appropriate. However, forpatients initiating PD because of transfer from

Table II-1. Peritoneal Dialysis Dose and Total SoluteClearance Measurement Schedule: Initial 6 Months

Month

PD Fluid PET Urine*

Kpt/Vurea CCr p Krt/Vurea CCr r

1† X X X X X2‡ Y Y3‡ Y Y4‡ X X X X5‡ Y Y6‡ X X X X

NOTE. X, measurement; Y, additional measurement if“incremental” PD utilized.

* For patients who void infrequently (�3 times in 24hours), collect urine over a 48-hour period.

† If possible, at the end of month 1, but at the end oftraining if that is more convenient.

‡ The measurement interval in months 2 to 6 is flexible.At least one additional measurement after the first month’smeasurement is necessary. If the results of the secondmeasurement are similar to those of the first measure-ment, an adequate baseline is established, obviating thethird measurement. If the result of the second measure-ment is discrepant, a third measurement is necessary toestablish a more reliable baseline.


HD and/or for patients who do not have substan-tial RKF, the first measurement of delivered doseof PD should be performed earlier. In the ab-sence of substantial RKF, waiting 1 month tomeasure delivered dose may result in inadequatedialysis for 1 month. Thus, the Work Grouprecommends that these patients undergo measure-ment of delivered dose of PD at 2 weeks postini-tiation, assuming maintenance exchange vol-umes have been achieved. Patient care techniciansmay be able to perform these measurements.

If “incremental” PD is initiated instead of “fulldose” (see Guideline 1: When to Initiate Dialy-sis—Kt/Vurea Criterion, and Appendix A, De-tailed Rationale for Guideline 1), RKF must befollowed carefully and frequently such that PDdose can be increased as RKF deteriorates. Whileurine production rate is presumed to be a clue todeteriorating RKF, that is not always the case.21

Thus, for patients initiating PD with “incremen-tal” PD, the Work Group recommends measuringRKF every 2 months. For patients on “full dose”PD, the Work Group recommends measuringRKF with total solute removal measurementsevery 4 months. If urine production rate is de-creasing, measure RKF every 2 months or asoften as needed and considered helpful, but atleast every 4 months. Once weekly Krt/V falls toless than 0.1, RKF can be considered negligibleand its routine measurement can be stopped.Guideline 11: Dialysate and Urine Collections,addresses this subject again.

GUIDELINE 4

Measures of PD Dose and Total SoluteClearance (Opinion)

Both total weekly creatinine clearance normal-ized to 1.73 m2 body surface area (BSA) andtotal weekly Kt/Vurea should be used to measuredelivered PD doses.

Rationale A valid and reproducible measureof PD dose is essential to assess the quantity ofdialysis delivered to an individual patient. Thequantity of dialysis is an important component ofthe quality of dialysis. Of the few availablemeasures of PD dose, total weekly Kt/Vurea andtotal creatinine clearance normalized to 1.73 m2

BSA are the best, because they are most stronglyassociated with mortality and morbidity (seeGuideline 15: Weekly Dose of CAPD). Addition-

ally, when properly performed, these measuresare reproducible enough to be useful in routineclinical practice.

The urea-based measure, Kt/Vurea, measuresremoval of the direct product of protein catabo-lism. The creatinine clearance (CCr) measuresremoval of a product of muscle metabolism,which provides insight into lean (ie, fat-free,edema-free) body mass and possibly into compli-ance (see Guideline 7: PD Dose Troubleshoot-ing). In Guideline 1: When to Initiate Dialysis—Kt/V Criterion, and Guideline 15: Weekly Doseof CAPD, there is a discussion of the comparisonof these two different measures. See Guideline 6:Assessing Residual Kidney Function, for a defi-nition of total weekly CCr.

These two recommended measures have bothbeen used to measure delivered dialysis dose.Since each measure provides slightly differentinformation, the Work Group recommends thatboth measures be used. Both creatinine and ureaconcentration can be obtained on the same sampleof urine, blood, and dialysate. No additionalsamples need to be collected to perform both,rather than one, of these measures. Most labora-tories perform both measures simultaneously (eg,6/60, Chem 6, etc) on automated equipment andthe cost is the same for one or both measures.

GUIDELINE 5

Frequency of Measurement of Kt/Vurea, TotalCCr, PNA, and Total Creatinine Appearance(Opinion)

After 6 months, total Kt/Vurea , total CCr , andPNA (with all its components) should be mea-sured every 4 months, unless the prescription hasbeen changed or there has been a significantchange in clinical status (see Table II-2).

Rationale Despite the establishment in 1993of ESRD Network/Health Care Finance Adminis-tration guidelines that measurements of deliveredPD dose and total solute clearance be performedtwice yearly, a Network Core Indicator review of1,208 patient charts in 1995 revealed that datasufficient to calculate such measures were availablefor only one third of the patients. The preliminary1996 results reveal that 69% of the patient chartshave such data (Diane Frankenfield, a member ofthe HCFA/HSQB ESRD Core Indicators PD Sub-committee, written communication, December 4,

MEASURES OF PERITONEAL DIALYSIS DOSE S73

1996; also available on the Internet at http://www.hcfa.gov/medicare/hsqb/hsqb1.htm).

Measurements of delivered PD dose and totalsolute clearance are easy to perform, but requireattention to detail and precision in technique forpatients and dialysis staff. A variety of clinicaland psychosocial events can interrupt and invali-date these measurements. It is imperative thatthese measurements become a routine for thepatients and facility staff. Setting a goal of per-forming measurements every 4 months buildsflexibility and leeway into a complex care plan,while assuring that a lengthy interval of possiblyinadequate PD does not occur. The 4-monthinterval between complete measurements of totalKt/Vurea, total CCr, and PNA is recommendedbecause it strikes a balance: every 4 months isoften enough to be clinically helpful, but not sooften as to be intrusive into a patient’s lifestyle orto create a burden for the dialysis facility. Aware-ness of loss of RKF must be paramount. If“incremental” PD is initiated instead of “fulldose” (see Guideline 1: When to Initiate Dialy-sis—Kt/V Criterion, and Appendix A: DetailedRationale for Guideline 1), RKF must be fol-lowed carefully and frequently such that PD dose

can be increased as RKF deteriorates. Whileurine production rate is presumed to be a clue todeteriorating RKF, that is not always the case.21

Thus, for patients initiating PD with “incremen-tal” PD, the Work Group recommends measuringRKF every 2 months (see Table II-2). For pa-tients on “full dose” PD, the Work Group recom-mends measuring RKF with total solute removalmeasurements every 4 months. If urine produc-tion rate is decreasing, measure RKF every 2months, or as often as needed and consideredhelpful, but at least every 4 months. Once weeklyKrt/V falls to less than 0.1, RKF can be consid-ered negligible and its routine measurement canbe stopped. Guideline 11: Dialysate and UrineCollections, addresses this subject again.

The impact of a change in prescription shouldbe assessed within 2 to 4 weeks in order todetermine if the recommended change has actu-ally been executed and if it has accomplished itsgoal. The promptness of the assessment is impor-tant because clinical events could occur in theinterval which could postpone the measurementor confound the results (see Guideline 10: Tim-ing of Measurement).

Some clinical events may impair the quality ofdelivered PD. A change in clinical conditionwhich warrants measurement of delivered PDdose is defined as any serious problem whichaffects nutritional status, the ability of the patientto perform PD mechanically or technically (suchas stroke or arthritis, loss of surface area fromsurgery, decreased exchange volumes due to her-nias, etc), or permanently affects the transportproperties of the peritoneum (eg, protracted peri-tonitis).22 Many conditions that lead to hospital-ization fall into one of these categories. Anysuggestion of exacerbation of uremia shouldprompt a measurement of delivered dose of PD.

The Work Group recognizes that technicalproblems in urine collections in some childrenmay justifiably decrease the frequency of urinecollections in selected cases.

GUIDELINE 6

Assessing Residual Kidney Function (Evidence)

Residual kidney function (RKF), which canprovide a significant component of total soluteand water removal, should be assessed by mea-suring the renal component of Kt/Vurea (Krt/Vurea)

Table II-2. Peritoneal Dialysis Dose and Total SoluteClearance Measurement Schedule After 6 Months

Month

PD Fluid Urine*

Kpt/Vurea CCr p Krt/Vurea CCr r

78 X† X†9

10 X X X X1112 X† X†1314 X X X X

NOTE. X, measurement.* If incremental PD is still being utilized at this point, the

frequency of RKF testing applies as described in Table 1 ofGuideline 3: Frequency of Delivered PD Dose and TotalSolute Clearance Measurement Within Six Months of Initia-tion. For patients who void infrequently (�3 times in 24hours), collect urine over a 48-hour period. Urine testingcan cease when the residual kidney function component isa weekly Krt/Vurea � 0.1.

† For young children who have greater difficulty withaccurate urine collection than adults, this may be deferreduntil full urine and dialysate collections occur every 4months (see Guideline 11: Dialysate and Urine Collection).


and estimating the patient’s glomerular filtrationrate (GFR) by calculating the mean of urea andcreatinine clearances.

Rationale A detailed rationale is presented inAppendix C. The following is a summary.

During the first few years of dialysis therapy,residual kidney function (RKF) contributes sig-nificantly to total solute and water removal. Pres-ervation of RKF may be particularly important tothe effectiveness of long-term PD. For soluteremoval targets to be met (see Guideline 15:Weekly Dose of CAPD, and Guideline 16:Weekly Dose of NIPD and CCPD) in manypatients without a possibly unacceptable dialyticburden, there must be a substantial contributionfrom RKF.

As GFR declines over time, the contributionof secreted creatinine to total creatinine clear-ance (CCr) rises disproportionately and CCr be-comes an inaccurate marker of GFR. Since theperitoneal membrane does not secrete solute, theGFR measure that corrects for creatinine secre-tion is the preferred measure to add to peritonealclearance. In the case of a low GFR, the measure-ment of GFR with endogenous solutes is bestdone by defining GFR as the arithmetic mean ofurea and creatinine clearance. This arithmeticmean essentially corrects for secretion of creati-nine. This GFR measure is added to peritonealCCr, normalized to 1.73 m2 of body surface areaand is totaled for a week. This is the “totalweekly creatinine clearance.”

GFR(mL/min)

�

kidney urea clearance(mL/min)� kidney creatinine clearance(mL/min)

2

Total weekly CCr � GFR � Peritoneal CCr

normalized to 1.73 m2 of Body Surface Area

The MDRD study derived two equations whichmay approximate GFR,23 which are noted inAppendix C.

An alternative measure of RKF is residualrenal urea clearance, normalized to total bodywater, Krt/Vurea. This measure can be directlyadded to the peritoneal urea clearance compo-nent, Kpt/Vurea, to create the total urea clearancenormalized to total body water, Kprt/ Vurea (short-ened to Kt/Vurea).

Creatinine clearance corrected for renal secre-tion and Kt/Vurea are both valuable measures inthe management of PD patients. Each measureoffers different information. Since the dialysateand urine collections are being performed foreither measure, the Work Group recommendsthat both measures be determined.

GUIDELINE 7

PD Dose Troubleshooting (Opinion)

In adult patients, a daily creatinine excretionin urine and dialysate that differs from the base-line rate (as determined during the first 6 monthsin Guideline 3, Table II-1) by �15% shouldprompt an investigation for noncompliance, im-proper collection of drained dialysate and/orurine, or altered peritoneal transport function.Compliance should not be assessed by compar-ing measured to predicted creatinine excretion.

Rationale Twenty percent of PD patients re-port some noncompliance with their dialysis pre-scription.3 Preliminary data suggest that totaldaily creatinine excretion or appearance can beused as an indicator of compliance in CAPD.The premise for such use is that, in noncompliantpatients who perform the proper number of ex-changes only during the day of the clearancemeasurement,24 the amount of creatinine ex-creted in 24 hours (equal to the daily amount ofcreatinine in the spent dialysate and urine plus anestimated amount of creatinine lost through otherroutes, primarily the gastrointestinal tract) willexceed the amount of creatinine produced daily.Essentially, noncompliance creates an unsteadystate of recently accumulated creatinine. Thus,an increase in the daily excretion of creatinine indialysate plus urine may indicate noncompliancejust prior to the collection.25 Other potentialcauses of variation in the measured amount ofcreatinine excreted include changes in musclemass (see Guideline 13: Determining Fat-Free,Edema-Free Body Mass), improper collection ofdialysate or urine due to timing errors, and inac-curate urine or dialysate creatinine measurementby the laboratory.25 Finally, another potentialcause of change in total creatinine excretion maybe peritoneal membrane transport dysfunction.Quantitatively, a very large transport defect mustoccur to result in 15% variation in the dailycreatinine excretion. However, if this is sus-


pected, a peritoneal equilibration test (PET) or itsalternative should be performed.

A similar approach should be considered inchildren, although only a small number of pediat-ric patients have been studied in this manner.26

Furthermore, in growing children with increas-ing muscle mass, there will be an increase intotal creatinine excretion over time.

The Work Group’s decision to use a varianceof �15% in creatinine appearance over the estab-lished baseline was based on convincing butindirect evidence in adult patients. There are nodata to support a similar approach in children. InPD patients who appear to be stable, creatinineappearance may vary by up to 15%, dependingon a variety of factors.27 This variance of �15%is simply a suggestion or warning to the clinicianthat the creatinine excretion data are not consis-tent with prior evaluations and suggests a needfor further investigation. The intensity of theinvestigation that the variance triggers is a clini-cal decision that requires taking many issues intoconsideration.

The Work Group does not recommend assess-ing compliance by comparing measured creati-nine excretion to predicted creatinine excretion.Our reasoning is as follows: The estimatedamount of creatinine lost in the gut is equal to0.036 � serum creatinine concentration in mg/dL � body weight.28 The predicted creatinineproduction, in mg/day, is calculated by theCockroft-Gault formulae29 as follows:

For men: [28 � (0.20 � Age)] � Weight

For women: [24 � (0.17 � Age)] � Weight

where age is in years and weight is in kilo-grams.24,30,31 These formulae were derived in anondialysis population. The discrepancy be-tween measured and predicted creatinine genera-tion is expressed as the ratio of measured/predicted creatinine generation.24

The use of a cut-off value of measured/predicted creatinine generation to identify non-compliance is not warranted because the mea-sured/predicted creatinine generation in compliantCAPD patients appears to vary widely.24,32,33 Inaddition, the increase in the amount of creatinineexcreted during the clearance day in noncompli-ant patients is very small in most cases.34-36

Measured/predicted creatinine generation is bet-ter used sequentially in a patient after establish-ing baseline values during a period of closeobservation (see Table II-1).32,36 At least for shortperiods of time (days or weeks), the steady-stateexcretion of creatinine is constant in CAPDpatients,33,37 although a variation of 15% may beessentially physiologic.27 However, since abso-lute creatinine excretion is being measured andcompared to a previously established reliablebaseline measurement, the Work Group consid-ers the use of predicted creatinine production tobe unnecessary.

In summary, the Work Group recommendsestablishing a baseline creatinine excretion onthe basis of 2 to 3 measurements in the first 6months of PD (see Guideline 3: Frequency ofDelivered PD Dose and Total Solute ClearanceMeasurement Within Six Months of Initiation).The Work Group feels that following these mea-sures longitudinally will be more helpful thancomparing measured to predicted creatinine ap-pearance. Causes for any subsequent deviationfrom the baseline total creatinine excretion overtime should be sought, recognizing that noncom-pliance is only one of several possible explana-tions.


Since preservation of RKF is important forsolute removal and contributes to total renalreplacement therapy, there is a need to identifycontributors to loss of RKF. For example, doantibiotics play a role? Hypotension? Other fac-tors? Does aggressive solute removal and/orhighly efficient dialysis remove stimulatory fac-tors favoring remnant kidney hyperfiltration?

Why does GFR vary so much on a day-to-daybasis and how does one account for this inadequacy studies? Is this a collection artifact ortrue physiologic variation? What factors alter thedaily production and excretion of creatinine? Is ita function of creatinine production or simplyexcretion? If the latter, is it variation in renalsecretion, filtration, or both? Urine output alsovaries dramatically on a day-to-day basis. Is thissimply a volume phenomenon or is it a reflectionof true clearance changes? Why does creatinineappearance vary even in compliant patients? In


children who are growing, how often should totalcreatinine excretion be measured and is it usefulas an assessment of compliance with dialysisprescription?

The recommendation that �15% variance in

creatinine appearance be considered as indica-tive of a status change or noncompliance shouldbe validated.

An accurate, reproducible, and easy-to-performmethod of measuring RKF should be developed.


III. Measurement of Peritoneal Dialysis Dose

GUIDELINE 8

Reproducibility of Measurement (Opinion)

Accurate measurement of total Kt/Vurea andtotal creatinine clearance (CCr) requires collec-tion and analysis of urine, dialysate, and serum ina way that yields reproducible and valid results.Dialysate creatinine concentration must be cor-rected for the presence of glucose in some as-says. Peritonitis precludes reliable measurementof delivered PD dose for up to a month. Compli-ance with complete collections is mandatory. Forpatients who void �3 times per day, a 24-hoururine collection is sufficient. For patients whovoid less frequently, a 48-hour collection is rec-ommended. For CAPD patients, the serum samplecan be obtained at any convenient time. ForNIPD patients, the serum sample should be ob-tained at the midpoint of the daytime emptyperiod. For CCPD patients, the serum sampleshould be obtained at the midpoint of the day-time dwell.

Rationale A detailed rationale is presented inAppendix D. The following is a summary.

Measurement of PD dose must be performedin a valid and reproducible fashion. The measureof creatinine concentration in effluent dialysatemust be corrected for the presence of glucosewith some creatinine assays. Each facility mustdetermine whether this is necessary by specifi-cally inquiring of its laboratory whether thecreatinine assay used by that lab is altered byhigh glucose concentrations. PD dose measuresshould not be made until a month after peritonitisresolves, because peritonitis causes residual ef-fects on membrane transport. Either total dialy-sate collections or aliquots (ie, samples of dialy-sate) can be used with proper patient training andcompliance. For CAPD patients, the timing ofthe blood sample is not important. For patientson NIPD or CCPD, the blood sample must reflectthe overall average for the entire 24 hours. ForNIPD patients, the serum sample should be ob-tained at the midpoint of the daytime emptyperiod. For CCPD patients, the serum sampleshould be obtained at the midpoint of the day-time dwell. For most NIPD and CCPD patients,these time points occur in the early afternoon.

GUIDELINE 9

Estimating Total Body Water and Body SurfaceArea (Opinion)

V (total body water) should be estimated byeither the Watson38 or Hume39 method in adultsusing actual body weight and by the Mellits-Cheek method38 in children using actual bodyweight.

Watson method38:For Men: V (liters) � 2.447 � 0.3362*Wt

(kg) � 0.1074*Ht (cm) � 0.09516*Age (years)For Women: V � �2.097 � 0.2466*Wt �

0.1069*HtHume method39:For Men: V � �14.012934 � 0.296785*Wt �

0.192786*HtForWomen:V� �35.270121 � 0.183809*Wt �

0.344547*HtMellits-Cheek method for children40:For Boys: V (liters) � �1.927 � 0.465*Wt

(kg) � 0.045*Ht (cm), when Ht �132.7 cmV � �21.993 � 0.406*Wt � 0.209*Ht, when

height is �132.7 cmFor Girls: V � 0.076 � 0.507*Wt � 0.013*Ht,

when height is �110.8 cmV � �10.313 � 0.252*Wt � 0.154*Ht, when

height is �110.8 cmBody surface area, BSA, should be estimated

by either the DuBois and DuBois method,41 theGehan and George method,42 or the Haycockmethod43 using actual body weight.

For all formulae, Wt is in kg and Ht is in cm:DuBois and DuBois method: BSA (m2) �

0.007184*Wt0.425*Ht0.725

Gehan and George method: BSA (m2) �0.0235*Wt0.51456*Ht0.42246

Haycock method: BSA (m2) � 0.024265*Wt0.5378

*Ht0.3964

Rationale A detailed rationale is presented inAppendix E. The following is a summary.

The Watson and Hume formulae were de-rived by comparing total body water measure-ments to simple anthropometric measurements(weight, height, age) in subjects without edema,volume deficit, or end-stage renal disease. Inperitoneal dialysis patients, the Watson andHume formulae provide reasonable approxima-tions of isotopic body water measurements.Volume abnormalities (edema) are apparently


the major cause of discrepancy. The Mellits-Cheek formulae were derived from subjectsaged 1 month to 34 years for males and 1month to 31 years for females. In each case,the measurement of total body water was per-formed in normal subjects by the use of deute-rium oxide distribution, with simultaneous mea-surement of weight and height.

The Work Group recommends the use of theWatson or Hume formulae in adults and theMellits-Cheek formula in children as methodsfor estimating V. Attention should be paid to thepresence of edema at the time of the clearancestudy. A special case is the underweight patient.(See Table II-1, Appendix E for a definition.)Successful efforts to restore weight to a normallevel in such a patient will result in a rising V andconsequently in a proportionally declining Kprt/Vurea. This does not alter the methodology ofestimating total body water using actual weight.It does affect target doses of dialysis, however.This issue is discussed again in Guideline 15:Weekly Dose of CAPD.

Like the formulae given above for total bodywater, the formulae for BSA were determined ina normal population. Many of the disclaimersdescribed for calculating V are less of an issue incalculating BSA, because the relationship to thedefining simple anthropometric measurements isless influenced by clinical conditions accompany-ing ESRD. Historically, many nephrologists haveutilized the method of DuBois and DuBois, andmuch of our data are from its application. Only 9subjects were used to define this formula.41 Morethan 400 subjects, including many children, wereused to define the formula of Gehan and George,42

and in an independent comparison, the Gehanand George method was preferred.44 The Hay-cock formula is based on measurements of 81subjects ranging from premature infants toadults.43

Amputation alters the relationship betweenbody height and weight. This causes a mathemati-cal distortion of the calculation of both anthropo-metric V and BSA, because the calculation ofeach takes this relationship into account.45,46

Modification of V and BSA in patients withamputations are described in detail in Appen-dix E.

GUIDELINE 10

Timing of Measurement (Opinion)

Routine measurements of total Kt/Vurea andtotal creatinine clearance should be performedwhen the patient is clinically stable (eg, stableweight, stable BUN and creatinine concentra-tions) and at least 4 weeks after resolution ofperitonitis.

Following a change in prescription or a majorchange in clinical status (eg, hospitalization,weight loss), but in the absence of recent perito-nitis, measurements of delivered weekly Kt/Vurea

and total weekly CCr should be performed withinthe next 4 weeks and then at 4-month intervals.

Rationale The effect of body weight on thecalculation of V is discussed in the rationale forGuideline 9: Estimating Total Body Water andBody Surface Area, and in Appendix E: DetailedRationale for Guideline 9. Variations in serumurea and creatinine concentration can potentiallyincrease the error in the clearance calculationsand indicate that the patient is not in a steadystate.

Peritonitis may, in some instances, affect peri-toneal solute transport for long periods. Therationale for waiting 4 weeks after resolution ofperitonitis to repeat the clearance studies is pre-sented in Appendix D: Detailed Rationale forGuideline 8.

The Work Group recommends frequent assess-ment of delivered dose of PD and total soluteclearance, specifically every 4 months after thefirst 6 months of PD (see Guideline 11: Dialysateand Urine Collections). Major changes in clini-cal status (eg, patient compliance, weight gain,weight loss, technical/mechanical complications,some causes of hospitalization) may alter PDdose requirements. For example, pneumonia maycontribute to loss of residual kidney function,which would be undetected unless measured.Therefore, in the absence of peritonitis, a majorchange in clinical status should prompt a re-evaluation of weekly Kt/Vurea and total weeklyCCr, and this should occur within 1 month follow-ing the change in clinical status. Within 1 monthfollowing a PD prescription change, weekly Kt/Vurea and total weekly CCr should be measured todemonstrate that the goals of the prescriptionchange have been achieved. If the patient is notstable, all attention should be directed to deter-

MEASUREMENT OF PERITONEAL DIALYSIS DOSE S79

mining the cause of the instability and to correct-ing it. This may or may not include measuringthe delivered dose of PD. There will be circum-stances in which the change in clinical statusmight only alter RKF (eg, exposure to nephrotox-ins), not delivered dose of PD. While one mustbe cautious in assuming that persistent urine flowrate implies stable RKF,21 a clinical clue thatdeterioration has occurred may be a decrease inwhat previously had been a stable daily urinevolume.47 In those settings, only measurement ofRKF is indicated.

GUIDELINE 11

Dialysate and Urine Collections (Opinion)

Two to three total solute removal measure-ments are required during the first 6 months ofPD (see Guideline 3: Frequency of Delivered PDDose and Total Solute Clearance MeasurementWithin Six Months of Initiation). After 6 months,if the dialysis prescription is unchanged:

1. Perform both complete dialysate and urinecollections every 4 months; and

2. Perform urine collections every 2 monthsuntil the renal weekly Krt/Vurea is �0.1.

Thereafter, urine collections are no longernecessary, as the RKF contribution to total Kt/Vurea becomes negligible. In young children, urinecollections are recommended only with com-plete dialysate collections (see Table II-2 repro-duced from Guideline 5).

Rationale Loss of residual kidney function isthe major cause of decreasing clearance in PDsubjects followed longitudinally.48,49 The CA-NUSA study demonstrated substantial loss ofkidney function at 6-month intervals.49 The WorkGroup concludes that measurements of urinaryclearances should be performed at 2-month inter-vals to prevent long periods of underdialysis. Foryoung children in whom urine collections aredifficult (requiring special collection apparatus,etc), urine collections can be deferred until thenext total solute removal measurement (seeGuideline 3: Frequency of Delivered PD Doseand Total Solute Clearance Measurement withinSix Months of Initiation, and Guideline 5: Fre-quency of Measurement of Kt/Vurea, Total CCr,PNA, and Total Creatinine Appearance).


The optimal timing of blood sampling forsubjects on asymmetric PD (NIPD, CCPD)should be determined. The recommendations wehave made are based on pharmacokinetic theory.

Comparison of the “batch” and “aliquot” meth-ods of dialysate sampling should be studied.

Development of a clinically applicable methodof assessing TBW in children undergoing PD isrecommended.

Methodology to calculate renal urea and creat-inine clearance and PNA from random urinesamples should be developed.


IV. Assessment of Nutritional Status Specifically as It Relates toPeritoneal Dialysis

GUIDELINE 12

Assessment of Nutritional Status (Opinion)

Nutritional status of adult PD patients shouldbe assessed on an ongoing basis in associationwith Kt/Vurea and Ccr measurements using theProtein equivalent of Nitrogen Appearance (PNA)and Subjective Global Assessment (SGA). Forpediatric PD patients, nutritional status should beassessed using the PNA and other standard nutri-tional assessments (see Guideline 14 of the Clini-cal Practice Guidelines for Peritoneal DialysisAdequacy and the K/DOQI Clinical PracticeGuidelines for Nutrition in Chronic Renal Fail-ure).

Rationale A detailed rationale is presented inAppendix F. The following is a summary.

There is strong indirect evidence linking sur-vival on dialysis with nutritional status both atinitiation of dialysis (see Section I: Initiation ofDialysis) and during longitudinal follow-up. Bet-ter survival has been reported in PD patients withhigh normalized protein equivalent of nitrogenappearance (nPNA)50 (see Guideline 28: Mea-surement of Normalized PNA in PD Patients).Positive correlations between nPNA and clear-ance of urea or creatinine have been reportedrepeatedly in PD subjects.51-54 The correlationbetween nPNA and Kt/Vurea may indicate in-creased appetite and dietary protein intake asKt/Vurea increases, but also may simply reflectthe fact that nPNA and Kt/Vurea are mathemati-cally linked.55 This mathematical linkage makesthe correlation between nPNA and Kt/Vurea incross-sectional studies of questionable clinicalsignificance. However, nPNA tends to increasein the same subjects when Kt/Vurea and creatinineclearance (CCr) are increased by increasing thedose of PD,53 especially if the increase in thedose of PD was prescribed because of inadequateclearances.56 In the latter instance, the associa-tion between Kt/Vurea and nPNA is not the resultof a mathematical coupling. In addition, there isstrong evidence suggesting that quality and quan-tity of dialysis influences nutrition.57,58 While theprecise relationship between kidney function (ordialysis therapy) and nutrition is not yet ad-equately understood, it is the Work Group’s opin-

ion that adequate renal replacement therapy isnecessary for normal appetite and metabolism.Thus, nutritional problems may reflect inad-equate dialysis which, if corrected, may lead tosubsequent improved outcomes.

Although nutritional status is influenced bymany nondialysis-related factors, appetite sup-pression, nausea, and vomiting are major clinicalfeatures of uremia and inadequate dialysis. There-fore, nutritional status is also an important mea-sure of PD adequacy. Of the available measuresof nutrition, PNA is recommended because itprovides an estimate of protein intake and pro-tein losses. The SGA is recommended because itis a valid clinical assessment of nutritional statusand is strongly associated with patient survival.

Protein equivalent of total nitrogen appear-ance (PNA) Nitrogen intake is almost entirelyfrom protein. The final product of protein catabo-lism is urea. Therefore, if steady-state nitrogenbalance conditions exist, one can work backwardfrom urea excretion to determine what the pro-tein intake was. Yet, other protein losses (urinary,peritoneal dialysate, diarrhea) also reflect thebody’s turnover of protein. Studies in dialysispatients show that predictable mathematical rela-tionships exist between urea excretion, proteincatabolism, and dietary protein intake. If perito-neal protein losses are greater than 15 g/day,PNA should be calculated as protein catabolicrate � protein losses. If dialysate protein lossesare less than 15 g/day, the formula:

PNA(g/d) � 10.76*(0.69*UNA � 1.46)

can be used to calculate PNA where UNA is totalurea nitrogen appearance in grams per day.58a

PNA is an indirect method for estimating dietaryprotein intake, a key measure of nutritional statusin dialysis patients. There are alternative Berg-strom formulae to obtain the PNA surrogate fordietary protein intake:

PNA(g/24 hours) � 15.1 �

(6.95 � urea nitrogen appearance in g/24h)

� dialystate and urine protein in g/24 hours59

American Journal of Kidney Diseases, Vol 37, No 1, Suppl 1 (January), 2001: pp S81-S83 S81

In the absence of direct measurement of urinaryand dialystate protein losses, this less accurateformula may be used:

PNA(g/24 hours) � 20.1

� (7.50 � urea nitrogen appearance in g/24 h)

When protein losses are high, this second for-mula should not be used. Both formulae willrequire normalization to body mass in kg.

Subjective global assessment (SGA) The SGAis a simple assessment that uses the clinician’sexperience to subjectively rate a patient’s nutri-tional status based on the medical history andphysical exam. The SGA was modified for use inPD patients as described in Appendix F: DetailedRationale for Guideline 12. This assessment isvaluable because it does not focus on a singlevariable; rather, it forces the clinician to view thepatient more broadly. SGA addresses four items(recent weight change, anorexia, subcutaneoustissue, and muscle mass) scored on a 7-pointLikert scale (see Appendix B: Detailed Rationalefor Guideline 2). It can be performed by physi-cians, nurses, or registered dietitians during rou-tine clinic visits. Several studies have validatedthat the SGA accurately reflects nutritional statusin dialysis patients and, in the CANUSA study, ahigher SGA was associated with a lower risk ofdeath.

The SGA is easy to perform and can be per-formed within minutes during a routine clinicvisit. There are no data to dictate how often toperform the SGA, so the Work Group bases itsopinion on the following: the SGA should bedone often enough to detect changes and tointervene in a timely manner. It should be per-formed in association with measurement of Kt/Vurea and CCr, every 4 months after the initial 6months (see Guideline 5: Frequency of Measure-ment of Kt/Vurea, Total CCr, PNA, and TotalCreatinine Appearance).

The SGA has not been validated as a means ofnutritional assessment in the pediatric PD popu-lation.

GUIDELINE 13

Determining Fat-Free, Edema-Free Body Mass(Opinion)

Total creatinine appearance should be used todetermine fat-free, edema-free body mass.

Rationale Fat-free, edema-free body mass isprobably a more accurate term for what hadpreviously been called lean body mass. It is animportant index of overall nutritional status. To-tal daily creatinine production, measured as thesum of creatinine excreted in dialysate and urineplus the estimated creatinine lost in the gut,28 canbe used to calculate fat-free, edema-free bodymass. Fat-free, edema-free body mass reflectssomatic protein stores in the same way thatserum albumin reflects visceral protein stores.60

In adults, fat-free, edema-free body mass inkilograms is computed by the equation60,61:

Fat-free, edema-free body mass � 0.029

� total creatinine production in mg/day � 7.38.

Norms vary by patient gender and size. Asteady-state of creatinine excretion should existfor the equation result to be valid. Factors otherthan muscle mass can affect the fat-free, edema-free body mass calculation by creatinine kinet-ics. These factors include errors in the collectionor measurement of creatinine in urine or dialy-sate and large variations in the dietary intake ofcreatine plus creatinine (meat). Fat-free, edema-free body mass estimates by creatinine kineticsmay be a better index of nutritional status in PDpatients, because they reflect dry fat-free, edema-free body mass and changes in muscle massbetter than dual-energy x-ray absorptiometry orbioimpedance.62 The day-to-day variability oftotal creatinine excretion is only 2% to 4% over ashort time interval,33,37 but is up to 15% overmuch longer intervals.27

Serum creatinine concentration is not, by it-self, an index of adequacy of peritoneal dialysisbecause of the large variations in creatinine pro-duction between individuals. However, a changein serum creatinine concentration may indicatechanges in creatinine and urea removal to a muchlarger extent than a change in serum urea concen-tration.63,64 A rising serum creatinine concentra-tion is usually caused by a decrease in totalcreatinine clearance, often secondary to a loss ofresidual kidney function, and much less fre-quently by an increase in muscle mass. A decreas-ing serum creatinine concentration is caused moreoften by progressive loss in muscle mass and lessoften by an increase in total clearance. In otherwords, increases in peritoneal solute transport or


recovery of kidney function do not occur veryoften.

GUIDELINE 14

Use of the Modified Borah Equation to AssessNutritional Status of Pediatric PD Patients(Opinion)

Nutritional status of pediatric PD patientsshould be assessed at least every 6 months bystandard clinical nutritional evaluations and bythe modified Borah equation65:

PNA(g/d) � [6.49*UNA] � [0.294*V]

� protein losses(g/day)

Rationale The equation described in Guide-line 12, Assessment of Nutritional Status, fromthe glossary65 is a further modification of theoriginal Borah equation.66 Since this modifica-tion has not been validated in children, the WorkGroup recommends using the modification abovefrom Kopple et al65 and Keshaviah et al.67

Although not validated in children, this modi-fied Borah equation contains a factor, V, thatcontrols for patient size, and has been employedin pediatric studies. Furthermore, dialysate pro-tein losses must be measured directly in thedialysis effluent and not estimated when usingthe modified Borah equation in children. The useof equations in which dialysate protein losses are

estimated has been studied in very few pediatricPD patients.68

The dialysate protein measurement is the onlyadditional laboratory determination from stan-dard total solute removal measurements, as de-scribed in Guideline 4: Measures of PD Dose andTotal Solute Clearance. Thus, this nutritionalassessment could be easily merged to accom-pany total solute removal measurements.


The precise relationships among PNA, dialy-sis dose, and outcome are unclear. Althoughthese relationships are currently being studied inhemodialysis patients, they should also be exam-ined in PD patients. There are probably limits,for example, to the role of increasing delivereddialysis dose in order to improve appetite andnutritional parameters. Other questions of inter-est include: How does improved dialysis affectnutrition, and above what delivered dose doesthat effect dissipate, if at all? What interventionsact synergistically with improved dialysis to im-prove nutritional parameters? What complica-tions interfere with nutrition, in what manner,and can the interference be overridden by an-other type of intervention?

A standardized nutritional assessment tool forchildren analogous to the SGA should be devel-oped.

ASSESSMENT OF NUTRITIONAL STATUS SPECIFICALLY AS IT RELATES TO PERITONEAL DIALYSIS S83

V. Adequate Dose of Peritoneal Dialysis

GUIDELINE 15

Weekly Dose of CAPD (Evidence)

For CAPD, the delivered PD dose should be atotal Kt/Vurea of at least 2.0 per week and a totalcreatinine clearance (CCr) of at least 60 L/wk/1.73 m2 for high and high-average transporters,and 50 L/wk/1.73 m2 in low and low-averagetransporters.

Rationale A detailed rationale is presented inAppendix G. The following is a summary.

Theoretical constructs predict that a weeklyperitoneal Kt/Vurea between 2.0 and 2.25 willprovide adequate dialysis. These constructs as-sume no residual renal function, full equilibra-tion of plasma and dialysate urea, a target serumurea nitrogen concentration between 60 and 80mg/dL, and nPCR between 1.0 and 1.2 g/kg/day.

Clinical studies addressing the validity of thesepredictions can be divided into those using uni-variate and those using multivariate statisticalanalyses. The former are methodologicallyweaker. Four studies which used univariate anal-ysis suggest that total (renal and peritoneal)weekly Kt/Vurea values greater than 1.5, 1.89,2.0, and 2.0, respectively, are associated withbetter patient survival than lower values.

Three studies from France, Italy, and NorthAmerica (CANUSA) have used multivariatestatistical analysis. The French study foundbetter survival among patients with an initialweekly Kt/Vurea �1.7 but did not evaluatechanges in Kt/Vurea associated with loss ofresidual kidney function. The Italian studyevaluated prevalent CAPD patients with mini-mal residual kidney function. Improved pa-tient survival was observed with a weeklyKt/Vurea �1.96. Values higher than 1.96 werenot associated with increased survival but thestatistical power to detect this association waslow. The CANUSA study of 680 incident con-tinuous peritoneal dialysis patients reported a5% decrease in patient survival in associationwith every 0.1 decrease in total weekly Kt/Vurea, for Kt/Vurea between 1.5 and 2.3. Therewas no association between Kt/Vurea and tech-nique failure or hospitalization. The predicted2-year survival associated with a constant totalKt/Vurea of 2.1 was 78%. These predictions

assume that renal and peritoneal Kt/Vurea areequivalent.

Clinical experience suggests that a total weeklycreatinine clearance �50 L/1.73 m2 is requiredfor adequate dialysis. Among patients with mini-mal residual function in the Italian study, a weeklyKt/Vurea of 1.96 correlated with a weekly creati-nine clearance (CCr) of 58 L. The CANUSAstudy reported a 7% decrease in patient survivalin association with a 5 L/1.73 m2/wk decrease inCCr. Unlike the situation for Kt/Vurea, both tech-nique failure and hospitalization were worse withdecreased weekly creatinine clearance. The pre-dicted 2-year survival of 78% was associatedwith a weekly Kt/Vurea of 2.1 or a weekly CCr of70 L.

There are insufficient data to address the issueof adequate compared to optimal dialysis (seeIntroduction). The latter is in part defined as thedialysis dose above which the incremental clini-cal benefit does not justify the patient burden orfinancial costs. Nor are there sufficient data toevaluate the relative importance of renal andperitoneal clearances. The recommendations as-sume equivalence but this requires further study.The correlation between Kt/Vurea and CCr willvary with residual renal function (see Fig II-2,Appendix A). The higher CCr observed in theCANUSA study compared to the Italian studywas due to the greater residual renal function inthe former.

Based on the available evidence, the minimumdelivered dialysis dose target Kt/Vurea should be2.0 per week; the minimum weekly target CCr

should be 60 L/1.73 m2. If there is discordance inachieving these targets, the Kt/Vurea should bethe immediate determinant of adequacy becauseit directly reflects protein metabolism and is lessaffected by extreme variations in residual renalfunction (see Appendix A and Fig II-2). How-ever, a cause for the discrepancy should besought and the patient followed closely for signsof underdialysis.

A special case is the underweight patient,defined in Appendix E: Detailed Rationale forGuideline 9. Successful efforts to restore weightto a normal level in such a patient will result ina rising V, and consequently in a proportion-ally declining Kprt/Vurea. To achieve a weekly


Kprt/Vurea of 2.0 at the increased weight, theweekly target Kprt/Vurea provided during themalnourished state must be greater than 2.0.The Work Group recommends that the targetKprt/Vurea should be raised in a malnourishedCAPD patient to the level that would provide aweekly Kprt/Vurea of 2.0 for that patient if he orshe were at the desired weight. That level iscalculated by multiplying the target of 2.0 forCAPD times the ratio of Vdesired/Vactual. This isdescribed in detail in Appendix E: DetailedRationale for Guideline 9, and discussed inGuideline 17: PD Dose in Subpopulations. Thesame upward target adjustment should be madein creatinine clearance. The target creatinineclearance should be adjusted upward by multi-plying the target for that therapy (CAPD orAPD) by the ratio of BSAdesired/BSAactual.

Even after controlling for delivered dose,low and low-average transporters have betterpatient and technique survival than do highand high-average transporters.69 In the absenceof adequate residual kidney function, low andlow-average transporters may not be able toachieve a CCr of 60 L/wk/1.73 m2 on anyreasonable dialysis prescription. However, be-cause urea clearance is less affected than creat-inine clearance by transport status, low andlow-average transporters can achieve a weeklyKt/V of 2.0. Therefore, it seems reasonable tolower the CCr target in low and low-averagetransporters without fear of jeopardizing pa-tient outcome. These patients must be ob-served closely for evidence of inadequate dialy-sis.

Clinical judgment suggests that the targetdoses of PD for children should meet or exceedthe adult standards. However, there are cur-rently no definitive outcome data in pediatricpatients to suggest that any measure of dialysisadequacy is predictive of well-being, morbid-ity, or mortality.69a There also are minimal dataregarding the real protein needs of children,especially young children, on dialysis.69b It isthe opinion of the Work Group that the nutri-tional requirements per kilogram of bodyweight are higher in children than in adults.Therefore, PD doses in children, and espe-cially small infants who have very high protein

requirements, may have to be higher than PDdoses in adults.

GUIDELINE 16

Weekly Dose of NIPD and CCPD (Opinion)

For NIPD, the weekly delivered PD doseshould be a total Kt/Vurea of at least 2.2 and aweekly total creatinine clearance of at least 66L/1.73 m2.

For CCPD, the weekly delivered PD doseshould be a total Kt/Vurea of at least 2.1 and aweekly total creatinine clearance of at least 63L/1.73 m2.

Rationale In the absence of data that relatedelivered dose of automated PD (APD) to patientoutcomes, targets for NIPD and CCPD are basedon opinion.

Theoretically, there is an 8% difference inclearance between CAPD and NIPD. This differ-ence is based on calculations which describe a200% increase in the intermittent HD clearancerequired to achieve the same solute removal as incontinuous dialysis (Kt/Vurea of 4.0 in HD and2.0 in CAPD), holding protein intake con-stant.70,71 The Work Group assumed that thedelivered dose of NIPD would need to be 8%higher than the CAPD dose (108% of 2.0 � 2.16,rounded up to 2.2). The Work Group assumedthat the requisite delivered dose of CCPD wouldbe intermediate between those for CAPD andNIPD. Some variations of CCPD with diurnalexchanges of less duration than the nocturnalexchange of CAPD may be considered equal toCAPD. However, in order to simplify recommen-dations, the target weekly total dose for CCPD is2.1. The recommendations for creatinine clear-ance are percentage adjustments correspondingto the changes in Kt/Vurea targets for these groups.

Clinical judgment suggests that the target dosesof PD for children should meet or exceed theadult target doses. There are no definitive out-come data in pediatrics to suggest that any mea-sure of dialysis adequacy is predictive of well-being, morbidity, or mortality.

GUIDELINE 17

PD Dose in Subpopulations (Opinion)

There is no adequate basis for recommendingany change in the target doses of dialysis dis-cussed in Guidelines 15: Weekly Dose of CAPD,

ADEQUATE DOSE OF PERITONEAL DIALYSIS S85

and Guideline 16: Weekly Dose of NIPD andCCPD, for various patient subpopulations (eg,patients with diabetes or who are elderly), withthe exception of the malnourished patient, whosetarget dose is increased by the ratio of the Vdesired/Vactual for Kt/Vurea. For creatinine clearance, thetarget dose in a malnourished patient is increasedby the ratio BSAdesired/BSAactual. Transport statusis not considered a subpopulation in the contextof this guideline.

Rationale There are no data available in theliterature on which to base a recommendation fordifferent adequacy targets for patients with diabe-tes or for the elderly. However, it must be remem-bered that malnourished patients may appear tohave an adequate Kt/Vurea due to calculation of Vfrom the actual or malnourished body weight. IfV were calculated from an estimate of desiredbody weight, the target would reflect that targetbody weight. This is discussed in Guidelines 9:Estimating Total Body Water and Body SurfaceArea, and Guideline 15: Weekly Dose of CAPD,and in detail in Appendix E: Detailed Rationalefor Guideline 9.

The fact that historically the size indicator tonormalize CCr is BSA and for Kturea has beentotal body water (V) contributes to the discrep-ancy between these clearance measures and con-founds population comparisons (male versus fe-male, obese versus lean, edematous versusnonedematous).

In the absence of data in these subpopulations,if no other cause of malnutrition is discovered,the target delivered dose of dialysis should beincreased by multiplying the target Kt/Vurea for anormally nourished patient by the ratio of theVdesired/Vactual, and the target creatinine clearanceshould be increased by the ratio of BSAdesired/BSAactual. These modifications are described inGuideline 15: Weekly Dose of CAPD, and Appen-dices E and G.

GUIDELINE 18

Use of Empiric and Computer Modeling of PDDose (Evidence)

Both empiric and computer modeling methodscan be used to estimate adequate doses of PD.Specific prescriptions are described below.

Rationale The Work Group has elected todescribe these two empiric and computer model-

ing approaches in detail. They are by no meansmutually exclusive.

EMPIRIC APPROACH FORDETERMINATION OF DOSE OF

PERITONEAL DIALYSIS

A. General Evaluation of the Patient WithKidney Failure

1. Explain all options (transplant, HD, andPD) to patients/parents/caregivers in a nonbiasedmanner.

2. Review medical condition/comorbidities todetermine if contraindications, relative or abso-lute, exist for any modality (see Section VIII:Suitable Patients for PD).

3. If no medical contraindications exist and thepatient is a candidate for self therapy, allowpatient to choose a modality.

4. Place the chronic dialysis access (PD orHD). The Vascular Access Work group recom-mends that vascular accesses be placed in pa-tients on PD. The PD Adequacy Work Groupfeels that this decision should be made on anindividual patient basis, but our position does notnecessarily disagree with the recommendationsof the Vascular Access Work Group.

5. If dialysis is needed at the time of presenta-tion, place the temporary HD access, or afterplacing the PD catheter, initiate therapy as sug-gested under point B.2, below.

B. Initiation of Peritoneal Dialysis

1. If possible, wait 10 days to 2 weeks aftercatheter placement to start PD.

2. If PD must be started in less than 10 daysfollowing catheter placement, do low-volume,supine dialysis.

3. Obtain baseline 24-hour urine collection forurea and creatinine clearance (see Guideline 6:Assessing Residual Kidney Function). These col-lections are for solute clearance calculations,assessment of creatinine generation, and PNAdeterminations.

4. Note patient’s weight and the presence orabsence of edema.

5. At initiation of dialysis, explain to patient/parents/caregivers that the patient’s prescriptionwill be individualized. Specifically, state thattheir instilled volume almost certainly will needto increase over time. For patients who choose


Automated Peritoneal Dialysis (APD), one ormore daytime dwells will be needed in approxi-mately 85% of patients. Patients should knowfrom the start of PD that their total solute clear-ance will be monitored and that, if their residualkidney function or peritoneal transport changesover time, their prescription may need to changeas well.

C. Initial Dialysis Prescription for Adults

Initial dialysis can be prescribed empiricallybased on patient’s weight, amount of residualkidney function, and lifestyle constraints. Theseempiric recommendations should be imple-mented prior to peritoneal equilibration testing.

PD may be initiated incrementally, or as fulltherapy, depending on RKF at the time of initia-tion (see Guideline 1: When to Initiate Dialysis—Kt/Vurea Criterion). For example, if Krt/Vurea is1.8 per week, only 0.2 Kpt/Vurea is needed perweek. Assuming complete urea equilibration (se-rum to dialysate) at 6 hours, a single 2-L over-night exchange would contribute 14 L per week.If V is 40 L, this contributes a Kpt/Vurea of 14/40or 0.35 per week. Any ultrafiltrate would addfurther to total solute removal. That, plus theKrt/Vurea of 1.8, brings the Kprt/Vurea to at least2.15, satisfying the target requirement. This ap-proach uses basic principles of dialysis prescrip-tion development. Thus, the dose of Kpt/Vurea

depends on the Krt/Vurea as the Work Group hasemphasized throughout these guidelines. Keep-ing in mind that the weekly Kprt/Vurea goal is atleast 2.0, the following more intense empiricapproach is reasonable:

1. Patients with an estimated underlying GFR�2 mL/mina. If patient’s lifestyle choice is CAPD:

BSA �1.7 m23 4 � 2.0 L exchanges/dayBSA 1.7 to 2.0 m2 3 4 � 2.5 L ex-changes/dayBSA �2.0 m23 4 � 3.0 L exchanges/day

b. If patient’s lifestyle choice is CCPD:BSA �1.7 m2 3 4 � 2.0 L (9 hours/night) � 2.0 L/dayBSA 1.7 to 2.0 m2 3 4 � 2.5 L (9hours/night) � 2.0 L/dayBSA �2.0 m2 3 4 � 3.0 L (9 hours/night) � 3.0 L/day

c. If patient’s lifestyle choice is NIPD:Specific attention to certain details willbe required. Nightly intermittent perito-neal dialysis (NIPD) is not a therapythat is typically used at the initiation ofdialysis. It has been reserved for high orrapid transporters. However, in patientswith significant RKF (and ability to di-urese), they may initially do well onnightly exchanges only (dry day) be-cause of the supplemental clearance pro-vided by the patient’s RKF. See furthercomments on NIPD under point 2.c,below.

2. Patients with an estimated underlying GFR�2 mL/mina. If patient’s lifestyle choice is CAPD:

BSA �1.7 m23 4 � 2.5 L/dayBSA 1.7 to 2.0 m23 4 � 3.0 L/dayBSA �2.0 m2 3 4 � 3.0 L/day (Con-sider use of a simplified nocturnal ex-change device to achieve optimal dwelltimes and to augment clearance.)

b. If patient’s lifestyle choice is CCPD:BSA �1.7 m2 3 4 � 2.5 L (9 hours/night) � 2.0 L/dayBSA 1.7 to 2.0 m2 3 4 � 3.0 L (9hours/night) � 2.5 L/dayBSA �2.0 m2 3 4 � 3.0 L (10 hours/night) � 2 � 3.0 L/day (Consider com-bined HD/PD or transfer to HD if clini-cal situation suggests need.)

c. If patient’s lifestyle choice is NIPD:Many of the issues discussed above for pa-

tients with an estimated underlying GFR �2mL/min still apply to urine volume. Namely, ifRKF provides enough diuresis, NIPD may pro-vide enough solute removal for a while. Thisshould be tested early on. If during training, it isnoted that a patient has very low drain volumeswith no apparent mechanical problem or leak, aPET should be done to determine if the patient isa rapid transporter. If so, NIPD can be prescribedusing kinetic modeling.

D. Initial Dialysis Prescription for Children

In view of the close, age-independent relation-ship between peritoneal surface area and bodysurface area (BSA), the use of BSA as a normal-ization factor for the prescribed exchange vol-ume in children is preferred. An instilled volume


of at least 1,100 mL/m2 is recommended formost pediatric patients, although individual toler-ance must be considered.72

It should be emphasized that the precedingprescriptive guidelines are general empiric guide-lines for patients initiating PD, generally as firstrenal replacement therapy. For patients transfer-ring from HD with minimal RKF, prompt ad-equacy testing is required. The above empiricrecommendations must be individualized andguided by documentation that the delivered doseequals the prescribed dose. Furthermore, the in-stilled volumes are ones that theoretically willresult in a weekly target Kt/Vurea of greater than1.9 for the average patient. Low transporters maybe below creatinine targets if RKF is low. Fi-nally, although most patients tolerate instilledvolumes of greater than 2.0 L, this needs to beevaluated for each patient.

E. Observations Needed During Training

1. Determine 4-hour drain volumes during train-ing. This is to note if drain volumes are asexpected for typical 4-hour dwells with 1.5%,2.5%, or 4.25% dextrose exchanges. This isnot a formal peritoneal equilibration test (seebelow), but is done to determine if the pa-tient’s peritoneal membrane transport charac-teristics are markedly different from the mean.

2. Monitor for evidence of leakage in the vicin-ity of the catheter.

3. Complete laboratory studies.a. Delay baseline peritoneal equilibration test

(PET) until after training (see F below).b. Perform serum chemistries and complete

blood count.c. If a computer-assisted kinetic modeling

system is available, enter preliminary datato predict if the current prescription will beadequate.

F. Early Follow-Up

1. Perform 24-hour dialysate and urine collec-tion for Kt/Vurea, creatinine clearance, PNA calcu-lation, creatinine generation, and D/PCreatinine andD/PUrea values. These should be done 2 to 4weeks following initiation (see Table II-1 andGuideline 3: Frequency of Delivered PD Dose

and Total Solute Clearance Measurement WithinSix Months of Initiation).

2. Perform peritoneal equilibration testing(PET) approximately 1 month following initia-tion of PD, an appropriate time physiologically.This baseline PET could be performed at the endof a prolonged (�1 week) training period (seeGuideline 3: Frequency of Delivered PD Doseand Total Solute Clearance Measurement WithinSix Months of Initiation). This PET (1 month) isused as the baseline measure of peritoneal mem-brane transport characteristics, not to determinetotal solute clearance. This PET is done to ruleout unsuspected problems or deviation from meantransport characteristics. Low transporters willprobably require high-dose CAPD or CCPD.High transporters will eventually have ultrafiltra-tion problems (when RKF diuresis fails) and willneed short-dwell therapy such as NIPD. Averagetransporters will have the most flexibility (ie, alloptions will be feasible).

3. Perform serum chemistries and completeblood count.

4. If a computer-assisted modeling program isavailable, enter baseline data. Actual data from24-hour collection can be compared.

5. If clearances are at or above target, con-tinue routine monitoring on a regular basis. Lookfor changes in 24-hour urine studies and PETdata. Kinetic modeling can be used to guidefuture therapy.

6. If clearance is below target at 1 month, achange in prescription may be needed. Compli-ance issues and collection procedures should beevaluated for abnormalities.

G. Adjusting Dialysis Prescription

If kinetic modeling is not available, unlessPET has changed, dialysis dose is most effec-tively increased by increasing the instilled vol-ume, therefore maximizing mass transfer anddwell time. Another option would be to increasethe number of exchanges/day while maintainingmaximum dwell time, ie, by using a single night-time exchange to increase to 5 equal dwells/day.To this end, simplified mechanical exchange sys-tems have been developed to perform a nocturnalexchange.

If kinetic modeling is available, use theseprograms to tailor a new prescription to meet


adequacy target goals and patient lifestyle issues.This is discussed in the next section.

COMPUTER-ASSISTED KINETIC MODELINGAPPROACH TO ACHIEVING TARGET DOSES

OF PERITONEAL DIALYSIS

As mentioned above, the availability of com-puter-assisted kinetic modeling to tailor PD pre-scriptions to transport type, body size, lifestyle,etc. may have distinct advantages. Much of whatis described in the preceding discussion of theempirical approach has a mathematical basis.Computer-assisted kinetic modeling is a logicalextension of the empirical approach in that ituses computer calculations to speed and assistthe physician in PD prescription development.PD solution manufacturers, such as Baxter andFresenius, provide urea kinetic modeling (UKM)models without charge.

The major advantage of this approach is theflexibility and speed of the calculations of soluteclearance. Recent studies have shown that cer-tain models very accurately predict dialysis deliv-ery.73-76 Kinetic modeling is especially importantfor APD therapies because the dwell times are sovariable and may not approach the optimal formany patients. Since the models accurately andreliably predict the delivered dose, the patientsand caregivers can discuss options in a timelymanner. The trial and error empirical approachdiscussed above moves at a much slower rate.Even with computer-assisted UKM, actual mea-surements are still necessary to confirm adequatedose delivery. But with computer-assisted UKM,the process is accelerated. The only theoreticaldisadvantage of a computer kinetic modelingapproach is that there might be a tendency for thecaregivers not to learn the principles behind themodeling program which form the basis for theprescription strategies.

The use of computer-based modeling toachieve target PD doses has been applied success-fully to a small number of children.77,78

The dose of PD is defined as the sum of thetotal daily or weekly kidney � peritoneal ureaclearance normalized to the total body water, theKprt/Vurea, which is a dimensionless parameterexpressed as either the total daily or weeklyfractional clearance of body water for urea.79,80 Itis substantially more difficult to compute theappropriate prescribed dialysis dose in PD than

in HD. In HD, Kt/Vurea is delivered in a singledialysis session and can be precisely calculatedfrom the dialyzer mass transfer coefficient(MTC), constant blood and dialysate flows, ultra-filtration rate, and treatment time.70,81 The deliv-ered Kt/Vurea and PCR (or PNA) can both becalculated from the predialysis and postdialysisBUNs from a single dialysis.70,81

In PD, however, the total daily peritonealclearance, Kpt, is comprised of the sum of theclearances provided by several discrete ex-changes. This therapy consists of several batchexchanges during which clearance and ultrafiltra-tion are not constant (unlike the situation in HD)but fall exponentially to zero over the course ofeach exchange. The peritoneal mass transfer co-efficient (MTC), which controls the rate of solutetransport between blood and dialysate (and henceclearance), is an individual patient characteris-tic71,82 which must be determined and which canclearly vary as a function of exchange volumeand body position.83,84 In HD, ultrafiltration con-tributes minimally to urea clearance, while in PDit contributes up to 25% or more of total clear-ance and must be included in calculation of thedose. The net ultrafiltration can be preciselycontrolled in HD, while in PD it is a complexfunction of glucose absorption, membrane waterpermeability and lymphatic flow. The PD pre-scription variables include MTC, which is depen-dent on patient, body position, and exchangevolume; distribution of exchanges between am-bulatory and supine cycler exchanges; exchangevolume(s); exchange times; and the osmotic gra-dient or percent dextrose in each exchange. Addi-tionally, residual kidney urea clearance must bemeasured and included in the prescription andbody water or V estimated from age, gender, andsurface area.39,85

In current clinical practice, the peritoneal dialy-sis prescription is usually based on transportcategorization using the peritoneal equilibrationtest (PET) and subsequently more finely tunedthrough empirical prescription changes guidedby clinical experience, as described in the preced-ing section of this guideline.

With computerized UKM many possible PDregimens with variable exchange schedules andvolumes can be tailored to be compatible withindividual patient lifestyle preferences and to


minimize total dialysate volume relative to re-quired Kprt/Vurea. A PD prescription can be quicklyand rigorously evaluated mathematically usingprograms written for the personal compu-ter.73-75,86 These programs all require baselinetransport characterization using either the PET orperitoneal function test data.

The most common method to monitor deliv-ered Kprt/Vurea is measurement of total dailyperitoneal and kidney urea clearance by analy-sis of blood, total drained dialysate, and 24-hour urine for urea nitrogen. Although highlyreliable for determination of Kprt/Vurea andPCR/PNA, batch analyses do not provide datato distinguish between noncompliance and/orpossible changes in MTC when the deliveredKprt/Vurea deviates from that expected with thecurrent prescription. There is further discus-sion of this subject in Guideline 7: PD DoseTroubleshooting, and Guideline 8: Reproduc-ibility of Measurement.

An alternative technique is measurement ofBUN, urine volume, and urea nitrogen in ali-quots of each exchange87 combined with thepatient’s report of the exchange time and vol-ume for each exchange. A further discussion ofaliquot methodology is in Guideline 8: Repro-ducibility of Measurement. Although this tech-nique, based on the peritoneal function testapproach, requires substantially more dialy-sate urea nitrogen measurements in addition tomeasurement of Kprt/Vurea and PCR (or PNA),it permits calculation of a MTC for each ex-change. If there are important deviations fromthe reported exchange schedule, the deviantexchanges will be identified by markedly devi-ant MTCs.

There are advantages and disadvantages ofboth the PET and PFT measurements. The widerange of exchange times, including nearly com-plete equilibration in long exchanges and theassumption of constant BUN, will result in somevariability in the MTCs measured with the PFTwhich do not reflect true differences. On theother hand, the MTC calculated with a single 2-Lexchange under carefully controlled conditionswill not always accurately reflect the MTC underclinical exchange conditions with variable ex-change volumes and body position.

A simple kinetic technique for routine monitor-

ing of delivered Kprt/Vurea and PCR/PNA in estab-lished patients for whom the MTCs for urea andcreatinine and 24-hour dialysate creatinine havebeen previously established is measurement ofBUN and serum creatinine and dialysate ureaand creatinine from an aliquot of one exchange.This data combined with the number of ex-changes, exchange times, and exchange volumesreported by the patient permits calculation ofKprt/Vurea, PCR/PNA, and expected total dialy-sate creatinine content.81 The validity of the datacan be assessed by comparison of the calculateddialysate creatinine content to the measured his-torical value for the patient (see Guideline 7: PDDose Troubleshooting). In this way, both Kprt/Vurea and PCR/PNA can be estimated from mea-surements of urea nitrogen and creatinine in ablood sample and a small aliquot of one ex-change using computerized UKM. When there isdeviation of more than 10% in the expectedcreatinine excretion, more complete dialysatecollections would be indicated for analysis oftherapy.


The amount of dialysis required for malnour-ished patients is not known. While there prob-ably is consensus that such patients need extradialysis, the requisite increase is unclear andshould be studied. Other malnutrition-relatedquestions of interest include: Can aggressivedialysis delivery reverse malnutrition? What V isto be used in malnourished patients?

Can increasing dialysis dose improve out-comes in a linear manner, or is there a dose abovewhich no benefit is noted, or complications orcosts outweigh the benefits?

A multicentered study of pediatric patients toevaluate clinical outcome as a function of deliv-ered PD dose should be initiated. Urea kineticmodeling computer programs specifically de-signed for children should be developed andvalidated in a prospective trial.

Although there is a database documentingthe validity of UKM to describe transport inPD,71,73-75,88,89 UKM has not been widely used toprescribe and control the delivered dose. Since therisk of mortality may be highly nonlinear withincreased dose of delivered dialysis,90,91 it is reason-able to assume that the coefficient of variation onmean Kprt/Vurea should not exceed 10% to 15% for


individual patients. A multicenter clinical trial tostudy clinical outcome as a function of Kprt/Vurea,using UKM to control Kprt/Vurea prospectively inindividual randomized patients is recommended.

Do patients with diabetes need higher targetsfor delivered dose of PD? Should PD delivereddose be increased in hospitalized patients duringacute illness or stress?


VI. Strategies for Increasing the Likelihood of Achieving thePrescribed Dose of Peritoneal Dialysis

GUIDELINE 19

Identify and Correct Patient-Related Failure toAchieve Prescribed PD Dose (Opinion)

Potential patient-related causes of failure toachieve prescribed peritoneal dialysis dose shouldbe investigated and corrected. These include:

● Failure to comply with the prescription.● Lack of understanding of the importance of

adherence to the full prescription.● Sampling and collection errors.Rationale A detailed rationale is presented in

Appendix H. The following is a summary.Preliminary data from the USRDS DMMS

Wave II project show that 487 CAPD patientsself-report full compliance with 82.8% of theirexchanges.3 One exchange/week is missed by11.5% of patients and 2 to 3 exchanges/week aremissed by 4.5% of patients, all self-reported. TheAmerican Association of Kidney Patients com-pleted a patient self-reported survey about theimpact of these DOQI guidelines and came upwith a very similar number for frequency ofmissed exchanges.

Conditions causing noncompliance in PD pa-tients have not been adequately analyzed. Fromstudies on compliance with chronic drug regi-mens, it is known that patients are more compli-ant when they are convinced about the appropri-ateness and beneficial effects of the prescribedtreatment and that frequent reinforcement of theimportance of the treatment is associated withbetter compliance. Therefore, it is the opinion ofthe Work Group that, in addition to giving care-ful consideration to the selection of medicallyappropriate candidates for PD, as detailed inSection VIII: Suitable Patients for PeritonealDialysis, special emphasis should be placed oneducation of PD patients about the importanceand technique of the PD prescription. Instruc-tions should be repeated at least every 6 months,and patients should be monitored for signs ofchange in compliance. Monitoring the output ofcreatinine in the dialysate plus urine, as detailedin Guideline 7: PD Dose Troubleshooting, isrecommended by the Work Group as a methodfor measuring compliance.

GUIDELINE 20

Identify and Correct Staff-Related Failure toAchieve Prescribed PD Dose (Opinion)

Potential staff-related causes of failure toachieve prescribed peritoneal dialysis dose shouldbe investigated and corrected. These include:

● Errors in prescription.● Inadequate monitoring of delivered dose.● Inadequate patient education.Rationale To increase the likelihood of

achieving a prescribed dose of PD, it is necessaryto elucidate the staff-related causes of failure toachieve a prescribed dose of peritoneal dialysis.The Work Group found no reports addressingthis issue in PD; the following discussion repre-sents the opinion of the Work Group members.

Inadequate understanding of the physiologyand kinetic principles of PD by the physiciansand nursing staff may result in:

● Errors in patient selection.● Errors in the prescription of the PD dose.● Errors in monitoring whether the prescribed

dose is delivered.● Errors in PD dose modification to achieve

the prescribed goal.● Inability to test for and recognize patient

noncompliance.● Inadequate patient education.The impact of patient education on patient

compliance with the PD prescription was dis-cussed in Guideline 19: Identify and CorrectPatient-Related Failure to Achieve PrescribedPD Dose. The chance of inappropriate prescrip-tion of the PD dose is enhanced when the pre-scribing physician has a sketchy knowledge ofthe principles of clearance studies in PD. It hasrecently been recognized that nephrology fellow-ship curricula lack emphasis on training in dialy-sis.92 To prescribe and deliver the proper dose ofPD, nephrologists must ensure adequate educa-tion and training in PD.

The use of computer modeling in PD may helpachieve the prescribed dose by suggesting vari-ous options to alter the PD dose. This approachmay assist in avoiding unrealistic PD dose sched-ules for certain patients (see Guideline 18: Use ofEmpiric and Computer Modeling of PD Dose).


The use of total creatinine appearance/outputdata in detecting noncompliance is important, asdiscussed in Section II: Measures of PeritonealDialysis Dose.

Inadequate education may be a key factor inthe patient nonadherence to the prescribed doseof therapy resulting in the above-mentioned short-cuts. The American Association of Kidney Pa-tients reports that PD patients are willing toincrease the frequency and/or volumes of ex-changes, if necessary, and that explanations (edu-cation) and participation in decision making aregood incentives. Inadequate education may stemfrom both poor educator understanding of theprinciples of clearance and lack of proper teach-ing technique. Staff responsible for patient educa-tion should be trained and competent in both the

principles of clearance and the technique ofpatient instruction.


Validate methods of assessing compliance.Evaluate the association between patient under-

standing of PD techniques and compliance. Spe-cifically, what is the role of inadequate patientknowledge in noncompliance?

Evaluate effect of staff’s knowledge of clear-ance principles and teaching techniques and rep-etition frequency of patient instruction on properdelivery of PD dose.

Is there a psychological profile which is predic-tive of noncompliance? If so, what is the bestmethod to characterize this profile?

STRATEGIES FOR ACHIEVING THE PRESCRIBED DOSE OF PERITONEAL DIALYSIS S93

VII. Clinical Outcome Goals for Adequate Peritoneal Dialysis

BACKGROUND

Throughout these Guidelines, the WorkGroup has focused on patient outcomes. Im-proving patient outcomes is the primary objec-tive of the K/DOQI (Kidney Disease Out-comes Quality Initiative). The Work Grouprealizes that definitions of goals regarding pa-tient outcomes are needed. As stated in theIntroduction to these guidelines, the goals areintegral to the definitions of adequate, optimal,and effective dialysis.

GUIDELINE 21

Measurement of PD Patient Survival (Opinion)

Survival of PD patients should be quantitatedserially as an outcome measure.

Rationale Patient survival is an objectiveoutcome that is dependent upon many vari-ables, some controllable and some uncontrol-lable. Suboptimal doses of delivered dialysiswill adversely affect patient survival in adults(data unavailable in children), as discussed indetail in Guideline 15: Weekly Dose of CAPD.A primary goal of ESRD therapy is to prolonglife while minimizing uremic symptoms. UnitedStates Renal Data Systems (USRDS) data fromhemodialysis patients have demonstrated anassociation between low Kt/V and increasedincidence of death from coronary artery dis-ease, other cardiac disease, cerebrovascularaccidents, and other conditions.93,94 There isalso evidence that underdialysis adversely af-fects mortality in PD patients with ischemiccardiac disease or left ventricular dysfunc-tion.16,95 Thus, patient survival is a measure ofrenal replacement program effectiveness. Casemix must be factored into survival analysis,however. The USRDS case mix analysis is anexcellent starting point, addressing age, race,primary renal disease, and presence or absenceof diabetes. The USRDS is attempting to refinecase mix further by addressing other underly-ing comorbidities. At dialysis centers with asmall number of patients, survival may need tobe evaluated over many years to obtain areliable estimate.

GUIDELINE 22

Measurement of PD Technique Survival(Opinion)

PD technique survival, both dependent andindependent of peritonitis, should be quantitatedserially in PD patients as an outcome measure.

Rationale It is common for ESRD patients tochange renal replacement therapy modalities dur-ing the course of their treatment. Reasons fortransfer include: complications of the therapy,inability to perform the therapy (lack of suitableaccess, no partner to do self care, medical contra-indication), and patient request/lifestyle issues.Patient case mix, geographical location, and ex-perience with PD in complicated cases are fac-tors affecting transfer. For some patients, foroptimal outcome, it may be medically appropri-ate to transfer from PD to HD; this does notimply failure of the therapy or the dialysis fa-cility.

Peritonitis remains the primary cause of trans-fer from PD. It is acknowledged that at timesperitonitis is the “precipitating” event for trans-fer, while the real underlying reason is patientburnout, noncompliance, inadequate dialysis, arequest based on lifestyle, or an underlying exitsite infection. Overall peritonitis rates can beinfluenced by the center. An association betweenmalnutrition and frequency of peritonitis hasbeen reported.96 Inadequate dialysis may lead toinadequate dietary protein intake and malnutri-tion as described in detail in Section IV: Assess-ment of Nutritional Status as it Relates to Perito-neal Dialysis. The relationship between soluteclearance and frequency or severity of peritonitishas not been adequately studied. For example, itis not clear if inadequate dialysis or malnutritiondirectly predispose the patient to peritonitis. How-ever, peritonitis is an important outcome and itsfrequency and severity is an index of the overallsuitability of PD. It is, therefore, the opinion ofthe Work Group that peritonitis should be moni-tored.

Inadequate dialysis is directly responsible forat least 10% of transfer to HD.93 There is anassociation between PD technique failure andtotal solute clearance,16,97 and one possible rea-son for poor technique survival rates may beunderlying inadequate dialysis. While the CA-


NUSA study found a relationship between creat-inine clearance and PD technique survival, theinvestigators suspected this was more related toRKF than delivered dose of PD. In the CANUSAstudy, technique survival was approximately 75%at 2 years in North America.16 However, peritoni-tis was not analyzed as a variable in the multivar-iate analysis. No difference was found in tech-nique survival between patients from Canadaand the United States. Average Kt/Vurea started at2.38 and decreased to 1.99 over 2 years. The riskof technique failure increased by 5% for every5-L/week decrease in creatinine clearance. Thesefindings corroborated data from Tattersall et al,97

who found that patients with a lower Kt/Vurea hada lower rate of technique survival. The lower rateof technique survival was related to underdialy-sis, not to peritonitis or hernia development. Thenutritional parameter of nPCR has been shown tobe predictive of CAPD technique failure in amultivariable analysis.98

It is a common perception that patients trans-ferring from any renal replacement therapy are atincreased risk for death in the immediate post-transfer period. However, indirect evidence fromthe USRDS does not support that perception.99

Early demise following transfer may be due to avariety of reasons, including the underlying causeof transfer, inadequate dialysis on PD, and mal-nutrition. Therefore, the Work Group recom-mends that technique survival be measured ateach PD facility. Admittedly, there may be center-specific differences for rates of transfer and thatat centers where there are small numbers of PDpatients, these rates may need to be evaluatedover many years. It is recommended that theserates be evaluated both dependent and indepen-dent of peritonitis, although, in one study (CA-NUSA), there was no significant difference be-tween the two evaluations.16

PD technique survival is dependent upon manyfactors including infections, patient motivation,ultrafiltration (transport characteristics), and to-tal solute clearance. Thus, PD technique survivalis not a simple outcome measure for the ad-equacy of PD. Nonetheless, centers should striveto achieve the goal of a 75% 2-year techniquesurvival rate (the rate noted in CANUSA). Casemix must be factored into survival statistics.

GUIDELINE 23

Measurement of Hospitalizations (Opinion)

ESRD-related and ESRD-unrelated hospital-izations (admissions/year, hospitalized days/year) in PD patients should be quantitated as anoutcome measure.

Rationale Hospitalization is an indicator ofthe overall effectiveness of treatment of chronicconditions and therefore constitutes an importantoutcome for dialysis patients. The number ofadmissions per year and total number of hospitaldays per year are two separate, but related, serialmeasures of outcome. Hospitalizations of PDpatients can be related or unrelated to ESRD. Anassociation between low creatinine clearance andincreased overall hospitalization rate has beenreported.16 Based on this evidence, the WorkGroup recommends that cause, frequency, andlength of hospitalizations of PD patients be moni-tored. Categorizing hospitalizations according towhether they are related to ESRD or not offerscertain advantages for analysis and, therefore, itis the opinion of the Work Group that this type ofstratified analysis should be performed.

According to the USRDS, PD patients arehospitalized an average of 1.8 times per year.100

The CANUSA study found, by multifactorialanalysis, an association between prolonged hos-pitalization and low creatinine clearance.16 Someadmissions are specific to PD, ie, not seen withother dialysis therapy, such as elective abdomi-nal wall herniography. As larger instilled vol-umes are administered to maintain target dosesof dialysis, there is an increased risk of leaks andhernia formation, both of which can lead tohospitalization. Admissions unrelated to ESRDare important indicators of morbidity (cardiacdisease, infections, etc) in PD patients. Sincehospitalization data are important outcome pa-rameters for all dialysis patients and can reflectsolute clearance, the Work Group recommendsthat they should be monitored.

Although it is uncertain whether inadequatedialysis is directly related to an increased risk ofperitonitis and catheter infections, inadequatedialysis is related to uremic symptoms such asnausea, vomiting, and gastrointestinal bleeding.It is acknowledged that some centers may treatall episodes of peritonitis in the hospital, whileothers only admit those with severe or refractory

CLINICAL OUTCOME GOALS FOR ADEQUATE PERITONEAL DIALYSIS S95

peritonitis. Therefore, in addition to trackinghospitalization rates, centers should also monitorreasons for hospitalization (related versus unre-lated to ESRD, and specific reason for admis-sion). The use of ICD-9 (International Classifica-tion of Diseases, 9th revision) or similar codesmay be valuable in this process. The USRDS isattempting to categorize causes of hospitaliza-tions as infectious, cardiovascular, dialysis access-related, and all other.

Hospitalizations from causes unrelated toESRD may be related to inadequacy of PD. Asdiscussed in Guideline 25: Measurement of PDPatient Survival, disease-specific (particularly car-diac) mortality is related to the dialysis dose forboth HD and PD. Therefore, although studies ofdisease-specific hospitalizations and their rela-tion to the dose of PD have not been reported, itis reasonable to monitor this relationship. Eachoutcome measure should be adjusted as well aspossible for case mix. The USRDS is attemptingto do so with Standardized Hospitalization Rates(SHRs).

GUIDELINE 24

Measurement of Patient-Based Assessment ofQuality of Life (Opinion)

Patient-based assessment of quality of life(QOL) in PD patients should be evaluated seri-ally as an outcome measure.

A patient-based quality of life instrumentshould have both generic and disease/treatment-specific measures of health-related quality of lifeand should be shown to be valid, reliable, andresponsive prior to use. Once such an instrumentis available, it should be administered at initia-tion of dialysis and at intervals determined to beappropriate by its validation studies.

Rationale Quality of life (QOL) can be as-sessed with generic or disease-specific measures.Many quality of life measures have been used indialysis patients. However, fewer measures havebeen used for peritoneal dialysis than for hemodi-alysis patients.101 Measures used in peritonealdialysis patients and reported in the literatureinclude101:

● Medical Outcomes Study Short Form 36(SF-36).

● Sickness Impact Profile (SIP).

● Index of Well Being, Index of Overall LifeSatisfaction.

● Index of Psychological Affect.● General Health Questionnaire.● Simmons Self Esteem Scale.● Profile of Mood States.● Multidimensional Health Locus of Control.● Modality Specific Stresses Scale.● General Treatment Stress Scale.● Global Illness Stress on Self and Others,

Global Adjustment to Illness Scale.● Quality of Life (QL 100 mm) Analogue

Scale.● Dialysis Relationship Quality Scale.● Social Leisure Activities Index, Social Sup-

port Satisfaction Scale.● General Well Being Index.● Index of General Affect, Overall Life Satis-

faction.● Katz Activities of Daily Living.● Time Tradeoff Measures.Unfortunately, many of these instruments do

not have published data indicating that reliability(test-retest, inter-rater), validity (content, con-struct, internal consistency), and responsiveness-to-change have been rigorously tested.100 Forthis reason, no particular instrument can bestrongly recommended over another. Further-more, many instruments developed for researchpurposes may be burdensome for patients orfacilities, eg, require interviewer assistance orhave complicated scoring algorithms. Neverthe-less, generic and disease-specific measures holdpromise as useful clinical tools.102

A popular generic measure used in peritonealdialysis patients is the Medical Outcomes StudyShort Form-36 (SF-36). Promising self-adminis-tered instruments used in peritoneal dialysis pa-tients include the CHOICE Health ExperienceQuestionnaire103,104 and the Kidney Disease Qual-ity of Life (KDQOL).105

The Work Group recommends that each facil-ity keep abreast of future developments regard-ing these instruments. As experience increasesand one or more instruments are clearly estab-lished as useful in PD patients, standardizedQOL measurement should be integrated into theroutine care and evaluation of patients, pro-grams, and facilities.


GUIDELINE 25

Measurement of School Attendance, Growth,and Developmental Progress in Pediatric PDPatients (Opinion)

School attendance (in the absence of othercomorbidities precluding school attendance),growth, and developmental progress should bemeasured serially in pediatric PD patients.

Rationale The ability of pediatric PD patientsto attend school is an important measure of thesuccess of PD.

Underdialysis may affect the cognitive devel-opment and statural growth of children. How-ever, the exact relationship between dialysis doseand normal growth and development in childrenis not clear. Nonetheless, the Work Group be-lieves that cognitive development and staturalgrowth should be monitored serially in childrenand charted in relation to patient age.

GUIDELINE 26

Measurement of Albumin Concentration in PDPatients (Opinion)

A stable or rising serum albumin concentra-tion that is greater than or equal to the lower limitof normal for each laboratory should be used asan outcome goal.

Rationale In PD patients, as with HD pa-tients, there is strong evidence to suggest that alow serum albumin level is associated with anincreased risk of technique failure anddeath.16,50,106,107 Patients with the highest serumalbumin levels have the lowest risk of death. Inthe CANUSA study, a difference of 0.1 g/dLserum albumin concentration was associated witha 5% change in the risk of technique failure, a5% change in days hospitalized, and a 6% changein the risk of death.16 Therefore, the Work Grouprecommends monitoring serum albumin concen-tration in PD patients because of its associationwith important outcomes.

Although the significance of serum albumin asa predictor of outcomes in adults is undisputed,its relationship to overall nutrition and, to alarger extent, to the levels of urea or creatinineclearance is unclear. That albumin synthesis de-pends on dietary protein intake is well known.However, catabolic illness can reduce albuminsynthesis, and probably increase albumin degra-dation, even when dietary protein intake is not

low. Observations in PD patients have providedindirect support for this effect of catabolic ill-ness. Although serum albumin concentration isan important predictor of outcome,50,106 it wasnot found to be significant in another study whencomorbid conditions were entered as covariatesin their model.107 In this last study, the presenceof comorbid conditions was associated with lowserum albumin.107 Several cross-sectional stud-ies have identified a positive correlation betweenserum albumin concentration and solute clear-ance.51,108,109 However, urea and creatinine clear-ance were not identified as predictors of serumalbumin by multivariate analysis.56,110 Age, co-morbid factors (diabetes), and peritoneal solutetransport were the major predictors of serumalbumin in these multifactorial analyses.

Normal serum albumin concentrations vary bylaboratory methodology; hence local standardsshould be used. If the serum albumin level isbelow normal for the laboratory, but is increas-ing, this suggests that the patient is anabolic andis increasing protein stores. Conversely, a lowalbumin or decreasing albumin level is likely tobe associated with malnutrition or decreasingprotein stores. Although there are no publisheddata specifically addressing this point, it is theWork Group’s opinion that a patient whose se-rum albumin has decreased 0.1 g/dL/month froma baseline of 4.0 g/dL to 3.7 g/dL may be athigher risk than a patient with a stable serumalbumin concentration of 3.7 g/dL.

Taken together, the data discussed above sug-gest to the Work Group that:

● Serum albumin concentration should bemonitored on a regular basis and a stable orrising value is desirable. It should be mea-sured at least every 4 months.

● Serum albumin levels should be evaluatedin the context of the patient’s overall clinicalstatus including comorbid diseases, perito-neal transport type, delivered dose of PD,and quality-of-life issues.

● The highest albumin level possible shouldbe the goal for each patient.

It is the Work Group’s opinion that an optimalserum albumin level can be obtained by adequatenutrition monitored frequently by the renal dieti-tian, prevention and treatment of catabolic ill-ness, and maintenance of Kt/Vurea and creatinine


clearance at or above the levels recommended inSection V: Adequate Dose of Peritoneal Dialysis.

In summary, low serum albumin is a strongpredictor of mortality and morbidity in PD pa-tients. Therefore, serum albumin is an importantoutcome measure in PD patients and should bemonitored, although an association between se-rum albumin and urea or creatinine clearance hasnot been convincingly shown. Efforts to main-tain serum albumin in the normal range shouldinclude adequate nutrition, adequate clearances,and prevention and treatment of catabolic illness.

GUIDELINE 27

Measurement of Hemoglobin/Hematocrit in PDPatients

Providers should strive to achieve a hemoglo-bin level of 11 to 12 g/dL or a hematocrit of 33%to 36% in 75% of PD patients.

Rationale See NKF-K/DOQI’s Clinical Prac-tice Guidelines for the Treatment of Anemia ofChronic Renal Failure.

GUIDELINE 28

Measurement of Normalized PNA in PDPatients (Opinion)

Providers should strive to achieve a normal-ized PNA (nPNA) of greater than or equal to 0.9g/kg/day in PD patients.

See Guideline 16 of the NKF/K/DOQI Clini-cal Practice Guidelines for Nutrition, which rec-ommends a dietary protein intake of 1.2 to 1.3g/kg body weight/day in clinically stable chronicperitoneal dialysis patients. Such a diet shouldlead to an nPNA equal to or greater than 0.9g/kg/day.

Rationale The role of PNA is discussed inGuideline 12: Assessment of Nutritional Status.

Maintenance of positive nitrogen balance andthe prevention of underlying malnutrition is im-portant because of the documented detrimentalimpact of hypoalbuminemia and low SGA scoreson patient survival.16,80,106,110 From nitrogen bal-ance studies, Blumenkrantz et al111 estimatedthat PD patients need to ingest at least 1.2 g/kg/dof protein to maintain positive nitrogen bal-ance.109 This is higher than the recommendeddaily protein intake for healthy individuals, butnot surprising due to the significant amount ofprotein known to be lost in dialysate. Despite

these recommendations from balance studies,Bergstrom et al53 and Nolph et al51 have reportedthat many patients are in positive nitrogen bal-ance with protein intakes of 0.9 to 1.0 g/kg/d.Cross-sectional studies would suggest that in theabsence of significant comorbid diseases, pa-tients with PD doses in the range of Kt/Vurea of2.0 spontaneously ingest at least 0.9 g/kg/d ofprotein.52,112,113 Total solute clearance and nPCR*are strongly correlated in cross-sectional stud-ies.57,114 However, it has been suggested that thisis due in part to mathematical coupling ofdata.55,115 Three studies have investigated theeffect of an increased Kt/Vurea on nutritional sta-tus (nPCR and serum albumin concentration) ina limited number of subjects.56,58,116 While nPCRincreased as Kt/Vurea increased, an increase inserum albumin concentration did not occur. Areasonable conclusion from these data would bethat in the absence of significant comorbidity, anincrease in delivered dialysis dose should resultin a corresponding increase in nPNA. In patientswho show signs of malnutrition, their dialysisprescription should be closely evaluated withconsideration to increasing their dose of dialysisif significantly below target. This is discussed inGuideline 15: Weekly Dose of CAPD.

No study of PD patients has demonstrated thatnPNA is an independent predictor of outcomewhen a multiple regression model is used. Corre-lation coefficients relating DPI to nPCR are onthe order of 0.6. However, PD patients who areneither anabolic nor catabolic tend to demon-strate higher correlation coefficients betweennPNA and DPI.53 Also, there are little data toshow a significant relationship between nPCRand serum albumin levels.56,110 Age, peritonealtransport type, presence of diabetes, and othercomorbid diseases have a greater effect on albu-min than does nPCR.

Despite these concerns, the Work Group rec-ommends that PNA should be monitored. LownPNA values in nonanabolic PD patients indicatea low DPI regardless of the values of other

*Studies that used the term PCR are cited in this rationale.Since the original study authors used the term PCR, thisrationale will use the term PCR when specifically describingresults from studies which used that term. However, theWork Group favors the term PNA.


nutritional indices.54 One should strive to achievean nPNA of at least 0.9 g/kg/day in adult PDpatients. PNA values at this level or higher arelikely to be associated with neutral or positivenitrogen balance in the absence of significantcomorbidity or dialysate protein losses.

While the recommended dietary allowance fornormal children is known, there are no definitivedata regarding the real protein needs of children,especially young children on dialysis.69b How-ever, clinical practice suggests that the proteinneeds of children on PD are greater than therecommended dietary allowance, in part relatedto dialysate protein losses. Current recom-mended protein intakes for children receivingPD, referenced for age are as follows117:

Age (Years) Protein Intake* for PD

0-0.5 2.9-3.00.6-1.0 2.3-2.41-3 1.9-2.04-6 1.9-2.07-10 1.7-1.811-14 1.7-1.815-18 1.4-1.5†19-21 1.3†

*Values are expressed in grams of protein/kg/day.†Based on growth potential.

Because dialysate protein losses may varywidely in children, individualized recommenda-tions for dietary protein intake may benefit frommeasurement of dialysate protein losses. Anequivalent amount of protein to replace dialyticlosses must be added to the recommended dailyallowance for normal children.118


The relationship between solute clearance andthe frequency and/or severity of peritonitis hasnot been adequately studied. Specifically, doesinadequate PD dose contribute to peritonitis?

Studies to assess whether an increase in nPNAis associated with an increase in serum albuminlevels, nutritional status, or improved survivalwould be valuable.

Studies to further define the relationship be-tween nPCR and outcome are needed. For ex-ample, the longitudinal follow-up of nutritionalstatus (determined by a variety of methods)will be more influential in improving under-standing of nutritional outcomes. Longitudinalstudies should be emphasized over cross-sectional studies.

The relationship between PD dose and out-come parameters in children needs definition.Studies of nutritional interventions are lackingand are encouraged.


VIII. Suitable Patients for Peritoneal Dialysis

GUIDELINE 29Indications for PD (Opinion)

Indications for PD include:● Patients who prefer PD or will not do hemo-

dialysis (HD).● Patients who cannot tolerate HD (eg, some

patients with congestive or ischemic heartdisease, extensive vascular disease, or inwhom vascular access is problematic, includ-ing the majority of young children).

● Patients who prefer home dialysis but haveno assistant for HD, or whose assistantcannot be trained for home HD.

● Rationale There is a rapid change in solutetransport as well as rapid shifting of volumewithin compartments during HD. Some pa-tients with severe cardiac disease may bebetter managed on PD since these acutechanges are avoided.119-123 PD has been pro-posed as a method of managing refractoryheart failure even in patients without renalfailure.124

Advantages of PD in patients with cardiovas-cular disease include: better hemodynamic con-trol, less acute hypokalemia (or electrolyte shifts)which could result in arrhythmia, and bettercontrol of anemia (important in patients withcoronary artery disease). Although a comparisonof PD to HD for patients with severe heart failurehas not been published, there are several reportsof successful PD performance in subjects withsevere heart failure.125-130 Tolerance of the proce-dure (PD), fluid management, prevention of ar-rhythmias, and patient survival were satisfactoryin these reports.

Extensive peripheral or central venous occlu-sive disease prohibits surgical placement of sometypes of hemodialysis access. Manifestations ofsevere ischemia, even gangrene, of the handsfollow placement of vascular access in the samewrist or forearm in a few patients with severeperipheral vascular disease, particularly diabet-ics.131 Marginal vascular beds are at risk forischemia or reduced perfusion during hypoten-sion, which is frequent in some HD patients.These patients benefit from increased vascularstability, which can be achieved with PD.

Over a period of time, vascular accesses failand revisions are no longer able to restore ad-

equate blood flow. As a result, the patient re-ceives inadequate hemodialysis and should beevaluated for PD.119,122,132

Home hemodialysis requires an assistant. Forpatients who prefer dialysis at home, the lack ofa hemodialysis assistant may mandate PD. Inaddition, patients who have transportation prob-lems to a hemodialysis center or live a greatdistance from a center may prefer home PD.133

The decision to initiate PD rather than HD inchildren is influenced by a variety of factors.Because of the difficulties in maintaining vascu-lar access in infants and small children, PD isusually the modality of choice when weight is�20 kg. Regular school attendance by childrenof all ages can best be achieved with a homedialysis procedure. PD is typically preferred overHD. Finally, renal replacement therapy can alsobest be provided by PD when the child lives along distance from a pediatric ESRD center.

GUIDELINE 30

Absolute Contraindications for PD (Opinion)

Absolute contraindications for PD include:● Documented loss of peritoneal function or

extensive abdominal adhesions that limitdialysate flow.

● In the absence of a suitable assistant, apatient who is physically or mentally inca-pable of performing PD.

● Uncorrectable mechanical defects that pre-vent effective PD or increase the risk ofinfection (eg, surgically irreparable hernia,omphalocele, gastroschisis, diaphragmatichernia, and bladder extrophy).

Rationale Documented Loss of PeritonealFunction. PD efficiency relies on effective perito-neal blood flow, dialysate flow, sufficient perito-neal surface area, and permeability to allowadequate solute and fluid removal. Any compro-mise in these functions may result in inadequateperitoneal dialysis and thus the failure of PD.120,134

It should not be assumed that children whohave previously undergone extensive abdominalsurgery will not achieve successful PD. A trial ofPD is warranted in such children and adequatedose delivery must be documented.

Psycho-Neurological Problems. The opti-mal performance of PD requires certain physical


and intellectual capabilities of the patient orcaregiver. With major loss of mechanical func-tion or eye-hand coordination, PD becomes diffi-cult to perform. Patients or caregivers are respon-sible for problem identification and problemsolving during PD. If the patient is deemedpsychologically incompetent, these tasks and de-cisions may not be reliably or safely ex-ecuted.122,133

Abdominal Mechanical Problems. The dia-lysate in the abdomen must be accessible to thevascular bed of the peritoneal membrane. Anymechanical problem that prevents this (eg, her-nia sack, subcutaneous leak) will impair theefficiency of PD. Intra-abdominal pressure in-creases with dialysate infusion and during theultrafiltration process, thereby exacerbating anystructural defect such as hernia. Some of theseabdominal defects are not surgically correct-able.122,123

GUIDELINE 31

Relative Contraindications for PD (Opinion)

Relative contraindications for PD include:● Fresh intra-abdominal foreign bodies (eg,

4-month wait after abdominal vascular pros-theses, recent ventricular-peritoneal shunt).

● Peritoneal leaks.● Body size limitations.● Intolerance to PD volumes necessary to

achieve adequate PD dose.● Inflammatory or ischemic bowel disease.● Abdominal wall or skin infection.● Morbid obesity (in short individuals).● Severe malnutrition.● Frequent episodes of diverticulitis.Rationale Fresh Intra-Abdominal Foreign

Bodies. Newly implanted abdominal prosthesesmust be allowed sufficient time for healing toavoid leakage or possible dialysis-related perito-nitis with potential spread to the prosthetic de-vice or material. The time required for healingmay vary from 6 to 16 weeks.135-137 The bacterialseeding of any vascular prosthesis during hemo-dialysis is also a risk. The best type of dialysis inthis setting is unclear.

Peritoneal Leaks. Peritoneal leakage intosubcutaneous tissues, pleural space, or genitaliacan be painful and cause local problems. Leakinginto the vagina or rectum increases the risk of

contamination. Unsatisfactory drainage and clear-ance, as well as medical complications, such asrespiratory compromise in the case of diaphrag-matic leak, can occur as a result of such leak-age.122,123,133

Body Size Limitations. Body size can be arelative contraindication to PD when the patientis either too small to tolerate the prescribeddialysate volume or too large to achieve ad-equate dialysis. For patients with little or negli-gible RRF, there are definite size limitations foradults on CAPD with 4 daily exchanges.138 How-ever, even larger individuals can achieve accept-able clearances if they are treated with a combi-nation of daily CAPD and nocturnal automatedPD.139 In large individuals, increase in the ex-change volume is more efficient than increase inthe number of daily exchanges. However, thepatient with the increased exchange volume mayexperience abdominal pain or discomfort, short-ness of breath, or loss of appetite as a result ofabdominal pressure.140

Intolerance to PD Volumes Necessary toAchieve Adequate PD Dose. Intolerance to aPD volume is generally not known until it isattempted. Frequent exchanges with small vol-umes, as observed during automated PD, maynot be able to provide an adequate delivered doseof PD. Raising volumes to the limit of tolerancemay be problematic in patients with advancedlung disease or patients with recurrent hydrotho-rax. Infrequently, this may be applicable to somepatients with polycystic kidney disease or severelumbo-sacral disk disease.

Inflammatory or Ischemic Bowel Disease.Inflammatory or ischemic bowel disease or fre-quent episodes of diverticulitis are relative con-traindications to peritoneal dialysis. It is reason-able to assume that there may be increased riskfor transmural contamination by enteric organ-isms in these circumstances.133

Abdominal Wall or Skin Infection. Abdomi-nal wall or skin infection can lead to contami-nation of the catheter exit site, tunnel, andperitoneal cavity through touch and cross con-tamination.122 The decision to use PD in pa-tients with a colostomy or ileostomy must beindividualized, since successful application ofPD has been described in such patients.

SUITABLE PATIENTS FOR PERITONEAL DIALYSIS S101

Morbid Obesity. Morbid obesity can posespecial dilemmas in peritoneal catheter place-ment, the healing process, and in providing ad-equate dialysis. The possibility that increasedcaloric absorption from the dialysate could leadto further weight gain should also be considered.

Severe Malnutrition. Wound healing is com-promised in severely malnourished patients. Self-dialysis such as PD may not be suitable for manyseverely malnourished patients because of inabil-ity to comply with the dialysis regime. Further-more, peritoneal protein losses may not be toler-ated.

Frequent Episodes of Diverticulitis. Diver-ticulitis during peritoneal dialysis often results inperitonitis. Peritoneal dialysis in patients withfrequent episodes of diverticulitis places thesepatients at higher risk for peritonitis.

GUIDELINE 32

Indications for Switching from PD to HD(Opinion)

The decision to transfer a PD patient to HDshould be based on clinical assessment, the pa-tient’s ability to reach HD dose target levels, andthe patient’s wishes. In particular, these patientsshould have vascular access addressed as ad-vised by the NKF-K/DOQI Vascular Access WorkGroup.

Indications for switching from PD to HDinclude:

● Consistent failure to achieve target Kt/Vurea

and CCr when there are no medical, techni-cal, or psycho-social contraindications toHD.

● Inadequate solute transport or fluid re-moval. High transporters may have poorultrafiltration and/or excessive protein losses(relative contraindication, obviously discov-ered after initiation and the first PET).

● Unmanageably severe hypertriglyceride-mia.

● Unacceptably frequent peritonitis or otherPD-related complications.

● Development of technical/mechanical prob-lems.

● Severe malnutrition resistant to aggressivemanagement (relative).

Patients should be informed of the risks ofstaying on PD at a level of adequacy below thatrecommended by their physician.

Rationale The above recommended indica-tions for switching a patient from PD to HD arebased on the following considerations:

Consistent Failure to Achieve Target Kt/Vurea

and CCr. Consistent failure to achieve thetarget total solute removal with proper PD pre-scription management should lead to evaluationof compliance issues and deterrents to appropri-ate performance of peritoneal dialysis exchanges.After all avenues have been explored, if social orphysical issues cannot be overcome, transfer toHD may be necessary as long as the same issuesdo not deter appropriate therapy (eg, adequateultrafiltration, single pool delivered Kt/Vurea of1.2 thrice weekly, etc) on this modality.134,141

Inadequate Solute Transport or Fluid Re-moval. Peritoneal solute transport determinedby PET affects both solute and fluid removal byPD. Obviously, peritoneal transport type is dis-covered after initiation of PD by the first PET.High transporters may have poor ultrafiltrationand/or excessive protein losses (relative contrain-dication). Excessive protein losses are those thatexceed the patient’s ability to compensate by anincrease in dietary protein consumption. How-ever, peritoneal urea and creatinine clearancestend to be adequate in high transporters. Manyhigh transporters with poor ultrafiltration can beeffectively dialyzed with short dwell periods anddaytime exchanges, but such a regimen maybecome too burdensome for the patient’s life-style.120,134,141 Low transporters usually have ad-equate ultrafiltration, but, when they are rela-tively large, may have inadequate peritonealclearance of creatinine, but not necessarily adecreased clearance of urea.63

Excessive protein losses can occur if the pa-tient’s underlying disease includes active nephro-sis, if the patient is a high transporter, or iffrequent peritonitis occurs. The resulting malnu-trition will increase the patient’s mortality andmorbidity. In some children who are activelynephrotic, protein losses may be successfullyreplaced by supplemental (eg, nasogastric, gas-trostomy) tube feedings.

There are medical complications that maydevelop or have been present prior to initiation of

GUIDELINES FOR PERITEONAL DIALYSIS ADEQUACYS102

dialysis, but these may become apparent onlyafter peritoneal equilibration testing and ad-equacy studies.

Inadequate solute transport documented bymeasures of Kt/Vurea and creatinine clearancemust be evaluated. If the maximum PD prescrip-tion has been reached (increases in volumes andfrequency of exchanges including use of noctur-nal cycling) or the procedure is no longer achiev-able due to lifestyle complications, hemodialysisas an alternative should be explored.120

These guidelines have defined adequate solutetransport with regard to urea and creatinine.However, the failure to adequately remove othersolutes such as potassium may require switchingto another form of renal replacement therapy.

Inadequate ultrafiltration is usually secondaryto high transport characteristics or a mechanicaldefect hampering catheter patency or drain-age.142 In rare instances, inadequate ultrafiltra-tion is associated with low peritoneal transportcharacteristics, probably due to a significant re-duction in the area of the peritoneal membrane,or secondary to increased peritoneal lymphaticflow.143

Unacceptably Frequent Peritonitis. The defi-nition of unacceptably frequent peritonitis has tobe individually determined for each patient. Such

considerations as the availability of hemodialy-sis facilities will inevitably play a role.

Unmanageably Severe Hypertriglyceridemia.Unmanageably severe hypertriglyceridemia, re-sulting from, or exacerbated by, the dextroseload intrinsic to the dialysate, may increase therisk for cardiovascular disease.

Development of Technical/Mechanical Prob-lems. Irreparable technical or mechanical de-fects, such as catheter malposition, resulting inaccess failure.

Severe Malnutrition Resistant to AggressiveManagement (Relative). Due to the continuousprotein loss associated with PD, malnourishedpatients must be aggressively evaluated andtreated. If treatment of malnutrition is not success-ful, transfer to HD is indicated.


The topic of suitability of patients for PD orHD has not been thoroughly investigated. Pro-spective comparisons of PD and HD for specificESRD patient categories (eg, those with severeheart failure, those with advanced malnutrition,those with large body size, etc) are needed todefine the subsets of ESRD patients which aremost suitable or unsuitable for PD.

SUITABLE PATIENTS FOR PERITONEAL DIALYSIS S103

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140. Beardsworth SF: The complications of peritonealdialysis, in Practical Peritoneal Dialysis. Bristol, England,John Wright & Sons, 1984, pp 63-69

141. Holley JL, Piraino B: Careful patient selection anddialysis prescription are required for effective nightly inter-mittent peritoneal dialysis. Perit Dial Int 14:155-158, 1994

142. Tzamaloukas AH, Saddler MC, Murata GH, Malho-tra D, Sena P, Simon D, Hawkins KL, Morgan K, NevarezM, Wood , Ellege L, Gibel LJ: Symptomatic fluid retentionin patients on continuous peritoneal dialysis. J Am SocNephrol 6:198-206, 1995

143. Mactier RA: Investigation and management of ultra-filtration failure in CAPD. Adv Perit Dial 7:57-62, 1991


X. Appendices

Appendix A: Detailed Rationale for Guideline 1

GUIDELINE 1

When to Initiate Dialysis—Kt/V urea Criterion(Opinion)

Unless certain conditions are met, patientsshould be advised to initiate some form of dialy-sis when the weekly renal Kt/Vurea (Krt/Vurea)falls below 2.0. The conditions that may indicatedialysis is not yet necessary even though theweekly Krt/Vurea is less than 2.0 are:

1. Stable or increased edema-free body weight.Supportive objective parameters for adequatenutrition include a lean body mass �63%, subjec-tive global assessment score indicative of ad-equate nutrition (see Guideline 12: NutritionalStatus Assessment, and Appendix B: DetailedRationale for Guideline 2) and a serum albuminconcentration in excess of the lower limit for thelab, and stable or rising; and

2. Nutritional indications for the initiation ofrenal replacement therapy are detailed in Guide-line 27 of the NKF-K/DOQI Clinical PracticeGuidelines on Nutrition, part of which are repro-duced as Guideline 2 of the PD Adequacy Guide-lines.

3. Complete absence of clinical signs or symp-toms attributable to uremia.

A weekly Krt/Vurea of 2.0 approximates a renalurea clearance of 7 mL/min and a renal creati-nine clearance that varies between 9 to 14 mL/min/1.73 m2. Urea clearance should be normal-ized to total body water (V) and creatinineclearance should be expressed per 1.73 m2 ofbody surface area. The GFR, which is estimatedby the arithmetic mean of the urea and creatinineclearances, will be approximately 10.5 mL/min/1.73 m2 when the Krt/Vurea is about 2.0.

Rationale In patients with chronic kidney dis-ease, progression of kidney failure should bemonitored by following total weekly renal ureanitrogen clearance (Krturea) normalized to ureavolume of distribution (V), ie, Krt/Vurea.1,2 Thisdoes not imply that a weekly collection of urineis necessary. A daily collection multiplied byseven yields a reasonable approximation ofweekly clearance. The knowledge of Krt/Vurea isespecially important when glomerular filtration

rate (GFR) falls below 25 to 50 mL/min, atwhich time spontaneous decrease in dietary pro-tein intake is commonly observed.3-6 The bloodurea nitrogen (BUN) and serum creatinine valuesshould not be used to monitor progression ofrenal failure, particularly in patients with diabe-tes.2 BUN may be low secondary to low proteinintake and may not adequately reflect the degreeof the renal functional impairment. Serum creati-nine may be low due to decreased muscle massas seen in some women, in the elderly, and inmalnourished patients. Hence, serum creatinineconcentration may not adequately reflect the de-gree of the renal functional impairment.

The estimation of V (total body water) by anyformulae has not been validated in children withrenal failure. Thus, the use of Krt/Vurea as anindication for the initiation of PD is recom-mended considering this caveat. Creatinine clear-ance as a means of assessing RRF for purposesof initiation of dialysis should be normalized tobody surface area (BSA).

An increasing body of evidence1,7-10 suggeststhat Krt/Vurea is a reliable predictor of outcome inPD and that weekly values in the range of 2.0provide adequate therapy (see Guideline 15:Weekly Dose of CAPD). Although the CANUSAdata indicated a linear decrease in modeled mor-tality rate with increasing Kprt/V up to 2.3, thereis some uncertainty about the significance of thehigh Kprt/V levels achieved in this study.11

It has always been a paradox that nephrolo-gists have insisted on optimal therapy once pa-tients are started on dialysis but have acceptedmuch lower levels of renal function, defined asKrt/Vurea, during the predialysis phase of patientmanagement. For example, while we recognizethat a weekly Kprt/Vurea of 2.0 or higher is associ-ated with improved outcome on PD, dialysis isusually not initiated until weekly Krt/Vurea is inthe range of 0.71 to 1.3.2,12 It is possible that theconsequences of delaying initiation of PD maybe analogous to the experience of the NationalCooperative Dialysis Study, wherein the mortal-ity rate in the year after the study ended wasmore than twice as high in those randomized tothe low dose dialysis protocols, even though they

American Journal of Kidney Diseases, Vol 37, No 1, Suppl 1 (January), 2001: pp S109-S133 S109

were returned to standard dialysis after complet-ing 24 weeks in the high BUN (low clearance)arm of the study.13

The Work Group feels that the data of Ikizleret al,4 McCusker et al,12 and Pollock et al6

strongly demonstrate the linkage between de-creasing kidney function and worsening nutri-tional status. In the CANUSA study, multipleestimates of nutritional status were associatedwith two estimates of RKF.12 Patients who startedPD at lower levels of RKF had a worse nutri-tional status than those who started at a higherlevel of RRF. CANUSA further demonstrated anassociation between the relative risk of death andworse baseline serum albumin concentration,worse time-dependent SGA, and worse time-dependent percent lean body mass.1 While anassociation between risk of death and nPCRcould not be demonstrated in the multivariateanalysis, several univariate analyses did demon-strate an association of individual estimates ofbaseline nutritional status with survival.

These data are consistent with the observa-tions of Bonomini et al14 who found that patientsstarting dialysis with a residual kidney creatinineclearance of �5 mL/min had a worse long-termoutcome than patients starting incremental hemo-dialysis with a mean residual kidney creatinineclearance of 11 mL/min.

From these observational data, it seems reason-able to draw the following conclusions:

Once Krt/Vurea falls below 2.0 per week orcreatinine clearance falls into the range of 9 to 14mL/min/1.73 m2, initiation of dialysis or trans-plantation15,16 should be strongly advised. Thepatient should be considered to be at increasingrisk with any further decreases in Krt/Vurea in theabsence of renal replacement therapy interven-tion. If dialysis is not instituted when Krt/Vurea

falls below 2.0, it is mandatory to document anegative inquiry for clinical signs or symptomsof uremia and that the following have not oc-curred: (a) more than a 6% involuntary reductionin edema-free usual body weight (%UBW) or toless than 90% of standard body weight (NHANESII) in less than 6 months; (b) a reduction in serumalbumin by greater than or equal to 0.3 g/dL andto less than 4.0 g/dL (see Nutrition Guideline 3),in the absence of acute infection or inflamma-tion, confirmed by repeat laboratory testing; or

(c) a deterioration in SGA by one category (ie,normal, mild moderate, severe; see NutritionGuideline 9 and Nutrition Appendix VI). WhenPD is initiated, the Kpt/Vurea could be increasedincrementally17-21 such that the combined valueof Krt/Vurea � Kpt/Vurea does not fall below thetarget level of 2.0 (see Fig II-1 and Guideline 15:Weekly Dose of PD). Alternatively, the initiationof “full dose” PD may be offered. Since residualkidney function (RKF) is such a crucial compo-nent of total solute removal utilizing the incre-mental initiation approach, more intense scrutinyof RKF is necessary. For initiation with full dosePD, less intense scrutiny of RKF is indicated.This is discussed in Guideline 3: Frequency ofDelivered PD Dose and Total Solute ClearanceMeasurement Within Six Months of Initiation,and Guideline 5: Frequency of Measurement ofKt/Vurea, Total CCr, PNA, and Total CreatinineAppearance, which address frequency of mea-surements.

In the CANUSA study,1 the weekly CCr equiva-lent to a Kprt/Vurea of 2.0 was 70 L/wk/1.73 m2.As will be clear later in this discussion, a CCr thishigh is indicative of residual kidney function,which was clearly present in the CANUSA pa-tients at initiation of PD.

CAPD is the only continuous chronic renalreplacement therapy with which to quantitativelycompare continuous residual kidney solute clear-ance. The Work Group strongly supports theopinion that the outcome data for a weeklyKt/Vurea of �2.0 are so compelling that using the

Fig II-1. Solute removal and initiation of PD. Ex-ample of tracking solute clearance measurements fora single patient over a 12-month period. The point atwhich incremental PD was initiated is indicated by thearrow.


same figure for initiation of dialysis justifies theunknown but presumably small risks of perform-ing peritoneal dialysis. Those risks include infec-tions and the possibility that increasing the lengthof time on PD contributes to eventual patient“burn-out.” If a patient is suspected to be at highrisk for these complications, PD may not be thebest choice for renal replacement therapy.

The Work Group recognizes that the patientwill play a major role in accepting the initiationof dialysis based on a certain “laboratory value.”It is the responsibility of the care providers tomake clear to the patient the rationale for initiat-ing dialysis when the above conditions becomeapplicable. Reasons to justify a delay in initiatingdialysis are listed above. These reasons shouldbe documented, if present.

The Work Group also recognizes that for manyclinicians, initiating dialysis based on Kt/Vurea isa new concept. Therefore, we have attempted toequate this to the traditional measure of ureaclearance, creatinine clearance, and GFR (esti-mated by the arithmetic mean of urea and creati-nine clearance).

What follows is an explicit quantitative ap-proach to the concept of renal urea clearance(Kr urea, mL/min). We recommend that adequatePD be considered to require:

Kprt/V � 2.0 per week (1)

where Kprt is total weekly peritoneal plus renalurea clearance. Guideline 15: Weekly Dose ofCAPD, explains the rationale for recommendingthat Kprt/V be 2.0 per week.

For the purpose of this discussion, Kr urea isconsidered equivalent to Kp urea and, therefore,

Kprt/V � 1.44*7*Kr urea/V, (2)

where 1.44 converts mL/min to L/day, whenKrt/V is 2.0.

2.0 � 1.44*7*Kr urea/V and (3)

Kr urea � 0.20*V (4)

Equation 4 shows that Kr urea must equal 0.2times V when Krt/V � 2.0. It is of interest tocompare this criterion to those developed inde-pendently22 for hemodialysis (HD). For twiceweekly (biw) HD, a coefficient has been devel-oped22 from urea kinetic modeling to convert

Kr urea, mL/min, to L of equivalent urea clearanceduring each twice weekly dialysis. The twiceweekly adequate level of Kt/Vurea

23 in HD is 1.85(double pool) and the coefficient to convert Kr urea

to equivalent urea clearance during dialysis is 9.0with units of L/treatment/mL Kr urea. Therefore,

1.85 � 9.0*Kr urea/V or (5)

Kr urea � 0.20*V (6)

Equation 6 for biw HD is identical to Equation 4for PD. For thrice weekly (tiw) HD the (doublepool) coefficient previously developed22 is 5.0,therefore,

1.0 � 5.0*Kr urea/V or (7)

Kr urea � 0.20*V (8)

Since Equations 4, 6, and 8 are identical, it isapparent that PD, biw HD, and tiw HD should allbe started when Kr urea � 0.20*V. For an averagepatient with V � 35 L, this defines a level ofKr urea � 7.0 mL/min. There are constraints onthe lower level of Kr urea for biw HD.22 As FigII-1 suggests, treatment could be started incre-mentally once weekly Krt/Vurea falls below 2.0.Typically, this would involve a single overnightexchange, intended to restore Kt/Vurea to 2.0 perweek. Ultrafiltration would not be needed sinceat this level of Krt/Vurea urine volumes are usu-ally adequate.

Levels of Residual Renal Creatinine Clear-ance, Cr Cr, mL/min At Which Dialysis Should BeInitiated. There are no Kr Cr criteria for HD,and the criteria defining the contribution of re-sidual kidney function (Kr Cr) to therapy are dif-ferent from the criteria defining the contributionof peritoneal creatinine clearance (KpCr) to thedose of therapy. The problem arises from theargument that tubular secretion of creatinineshould be subtracted from the total kidney creat-inine clearance, and renal function with respectto creatinine clearance is best expressed as “GFR”as developed below. Therefore, the definitionsused with respect to Kr Cr will each be consideredseparately and related to the level of Kt/Vurea forwhich Kr urea and Kp urea are considered simplyadditive.

In all instances, the total weekly CCr is normal-ized to 1.73 m2 of BSA. In order to compare thisto the Kprt/Vurea, BSA must be normalized rela-

APPENDICES S111

tive to V, eg, based on the Hume equations andtaking the mean of the genders, 1.73 m2 � 35L.24 It is also reasonable to extend this as a linearrelationship over the domain of patient size al-though it should also be considered a gender-dependent relationship.

Consideration of Renal Contribution to DoseExpressed as Cr Cr. As noted above, in all casesthe dose of total creatinine clearance is expressedas L/wk/1.73 m2 of BSA. The following willnormalize total creatinine clearance to 1.73 m2

(nBSA) and Kt/Vurea to a standard V � 35 Lcorresponding to 1.73 m2 of BSA in order todevelop constants relating the creatinine andurea-based dosage parameters. To the extent thatBSA and V increase and decrease at the sameratio (reasonably valid), the constants developedare generalizable, and therefore, the relation be-tween Kr Cr and nBSA can be expressed as fol-lows:

[Kr Crt/nBSA] � 1.44*7*Kr Cr � 10.1 � Kr Cr (9)

Equation 9 simply describes the total weeklyliters of renal creatinine clearance as a functionof Kr Cr and our normalized BSA of 1.73 m2.

For the Kt/Vurea normalized to V � 35, there-fore,

Krt/nVurea � 1.44*7*Kr urea/35 � 0.29*Kr urea (10)

and, therefore,

Kr urea � 3.47*Krt/nVurea (11)

Assuming

Kr Cr � 2*Kr urea, (12)

we can substitute Equation 11 into Equation 12to show

Kr Cr � 2*3.47*Krt/nV � 6.94*Krt/nVurea (13)

Substituting now Equation 13 into Equation 9yields the following equation:

[Kr Crt/nBSA] � 10.1[6.94(Krt/nV)]

� 70(Krt/nV) (14)

Equation 14 shows that if we define the renalcontribution to PD therapy by Kr Cr, the level ofweekly Kr Cr per 1.73 m2 must be 70 times theKrt/nVurea so at Krt/nVurea of 2.0, Kr Cr t/1.73 m2 is140. For the average patient with V � 35 L and

BSA � 1.73 m2, the required level of Kr Cr � 14mL/min.

Consideration of Renal Contribution to DoseExpressed as “GFR.” In this case the effectiverenal creatinine clearance, eKr Cr, is defined as:

eKr Cr � GFR � [Kr Cr � Kr urea]/2 (15)

Therefore,

[eKr Crt/nBSA] � 1.44*7(Kr Cr � Kr urea)/2

� 5.0*Kr Cr � 5.0*Kr urea

(16)

Substituting from Equations 11 and 13, yields

[eKr Crt/nBSA] � 5*6.94(Krt/V)

� 5*3.47(Krt/V) � 52(Krt/V)(17)

Equation 17 shows that if the renal contributionto PD therapy is defined as GFR, which isequivalent to “effective” creatinine clearance oreKr Cr, the total weekly eKr Cr required relative toKrt/Vurea is 52 L/week/1.73 m2 per unit of Krt/Vurea. It can also be noted that in all instancesthese equations also relate to Kprt/Vurea and Kpt/Vurea since we have defined Kr � Kp.

Consideration of Peritoneal Creatinine Clear-ance to PD Dose. In this case, the dose mustbe expressed directly in terms of peritoneal creat-inine clearance (KpCr) and by definition,

[KpCrt/nBSA] � 1.44*7*KpCr � 10.1 KpCr (18)

The average relationship between KpCr and Kp

urea in CAPD is

KpCr � 0.8*Kp urea (19)

Since Kp urea � Kr urea and Kp ureat/nV � Kr ureat/nV, Equations 18, 19, and 11 can be combined toderive

[KpCrt/nBSA] � 28[Kp ureat/nV] � 28[Kr ureat/nV](20)

Equations 14, 17, and 20 show that the Creati-nine Dose Equivalency with respect to the singleurea Kprt /V criterion will vary widely dependingon how RRF is defined. The relationships areplotted in Fig II-2: Dose of PD With Respect toWeekly Creatinine Clearance Relative to WeeklyKprt/V, where the weekly creatinine clearancerequired per 1.73 m2 corresponding to a weeklyKprt /Vurea of 2.0 ranges from 140 to 56 L,


depending on the definitions used. There is noproblem in either the case of pure residual kidneyfunction with no PD therapy or the case of pureperitoneal dialysis with no residual kidney func-tion present. The problem arises when one at-tempts to sum residual kidney creatinine clear-ance with peritoneal creatinine clearance. In thiscommon circumstance, the dialysis dose relation-ship will be bounded by regression lines 2 and 3in Fig II-2.

For line 1, which defines creatinine clearanceas the uncorrected (for secretion) creatinine clear-ance, the creatinine clearance that is equivalentto a Kt/Vurea of 2.0 is 140 L/wk/1.73 m2. Line 2defines creatinine clearance as the mean of ureaand creatinine clearance, and the equivalence toa Kt/Vurea of 2.0 is 104 L/week/1.73 m2. Line 3represents all clearance from PD (complete ab-sence of residual kidney function). Under thiscondition a Kt/Vurea of 2.0 is equivalent to acreatinine clearance of 56 L/wk/1.73 m2.

This creates an irreconcilable ambiguity withrespect to the creatinine and urea dosage criteriafor defining optimal dialysis and the study ofoutcome as a function of dose. Because thepractice of PD has used both CCr and Kt/V toquantify delivered dose and there is a large bodyof literature describing outcomes related to CCr,the Work Group recommends continuing to useboth measures (see Guideline 4: Measures of PDDose and Total Solute Clearance). However, inview of this ambiguity, the Work Group recom-mends that if only one measure is to be utilized,use Kprt/Vurea rather than Kr Crt (see Guideline 15:Weekly Dose of CAPD). Nonetheless, creatinine

kinetics as discussed in Guidelines 4, 6, and 17are useful for estimating edema-free, fat-freebody mass, compliance with dialysis prescrip-tion, and some programs may prefer it for quanti-fication of delivered dose of PD. Thus, totalcreatinine excretion is valuable.

Finally, it is worth emphasizing that the basicrelationship between the level of residual Cr Cr toKr urea for initiation of dialysis will be the samefor all of these creatinine dosage criteria. Theyare related to Kprt/V since Kr Cr � 2 Kr urea and allof the expressions ultimately reduce to this rela-tionship.

Another way to view the creatinine clearanceat which to initiate dialysis is to extrapolatebackward from the CAPD target of 60 L/week/1.73 m2 (see Guideline 15: Weekly Dose of PD).This approximates a purely filtered only creati-nine clearance of 6 mL/min. Since at this level ofresidual renal function much of the creatinineappearing in the final urine is from tubular secre-tion, 60 L/wk/1.73 m2 approximates a total re-sidual renal creatinine clearance of 9 to 14 mL/min.

Peritoneal Dialysis and Residual Kidney Func-tion Equivalency. Quantitative replacement ofrenal urea clearance by peritoneal clearance isbased on the assumption that the two clearanceparameters confer equal clinical benefit withrespect to control of uremic morbidity. Thus, wecan write the relationship

Kprt/Vurea � Kpt/Vurea � Krt/Vurea, (21)

where Kpt/Vurea is total daily or weekly perito-neal urea clearance normalized to V; Krt/Vurea istotal daily or weekly renal urea clearance normal-ized to V.

Solution of Equation 21 for Kpt/Vurea with theassumption that adequate weekly Kprt/Vurea is 2.0results in

Kpt/Vurea � 2.0 � Krt/Vurea (22)

Equation 22 provides a quantitative guideline forreplacing residual renal urea clearance by perito-neal clearance such that the sum of weeklyKpt/Vurea and Krt/Vurea remains 2.0.

The equivalence of peritoneal and residualrenal clearance is controversial. Current datasuggest inconsistent conclusions. There is a strongsuggestion that protein metabolism in CAPD

Fig II-2. Dose of PD with respect to weekly creati-nine clearance relative to weekly Kprt/V. The dose ofPD with respect to weekly creatinine clearance relativeto weekly Kprt/V varies widely depending on the defini-tion of renal creatinine clearance.

APPENDICES S113

patients is similar to that in patients with chronickidney failure.24 Peritoneal clearance has beenshown to predict survival.25,26 However, a largeretrospective analysis suggested that peritonealclearance was not predictive of survival, whileresidual renal clearance was27 and indirect obser-vations seem to corroborate that. Thus, the WorkGroup will continue to equate residual renal andperitoneal clearance. To that end, the preserva-tion of residual renal clearance is paramount andstrategies to achieve this have recently beendescribed.28

Hemodialysis and Residual Kidney FunctionEquivalency. Compared to CAPD it is morecomplex to calculate incremental doses of HDsuch that the sum of intermittent dialyzer clear-ance (Kdt/Vurea) and continuous Krt/Vurea remainconstant at a level equivalent to a weekly Krt/Vurea of 2.0. However, the dose and frequency ofHD which provide therapy equivalent to continu-ous Kpt/Vurea can be calculated using the funda-mental assumption underlying CAPD therapy:the level of continuous Kpt/Vurea required fortreatment which is clinically equivalent to inter-mittent HD is that Kpt/Vurea which results in asteady state BUN equal to the average predialy-sis BUN with any specific intermittent HD treat-ment schedule at the same nPCR.29-32 From thisbasic assumption and the urea kinetic model19

the dose and frequency of HD required for incre-mental replacement of Krt/Vurea as it falls below2.0 can be readily calculated, as depicted inFig II-3.

The dose of intermittent HD is expressed inFig II-3 as eKdt/Vurea, which is the equilibrated,delivered, and normalized hemodialysis dose (seethe NKF-K/DOQI Clinical Practice Guidelinesfor Hemodialysis Adequacy for further discus-sion of eKdt/Vurea). The equilibrated measure isutilized here because in peritoneal dialysis, tran-scellular urea equilibration is achieved, and there-fore, it makes conceptual sense to think in termsof equilibrated values. From preliminary data ofthe HEMO study, eKdt/V is approximately 0.21lower than that computed from immediatepost-HD BUN sampling, using single-pool, vari-able volume kinetic modeling.33 The dashed linedepicts incremental increase in daily Kpt/Vurea asKrt/Vurea falls in accordance with Equation 22.Model solutions are shown for once, twice and

thrice weekly hemodialysis (N � 1, 2, and 3,respectively). The model solutions are limited toeKdt/Vurea �2.0 since it is unrealistic to prescribeeKdt/Vurea �2.0. Such a dose would correspondto single pool Kdt/Vurea values of 2.8 and 2.3 withtreatment times (t) of 2.0 and 4.0 hours, respec-tively. It can be seen that when N � 1, eKdt/Vurea � 2.0 when Krt/Vurea � 1.6. Thus, theoption for once weekly hemodialysis is limitedto a weekly Krt/Vurea �1.6. If Krt/Vurea � 0.5 andN �2, the eKdt/Vurea for each HD treatment mustbe 2.0 to achieve a weekly continuous Kt/Vurea

equivalent to 2.0. Therefore, for a weekly Krt/Vurea �0.5, more than twice weekly HD will benecessary. Finally, in the case of N � 3, eKdt/Vurea increases linearly to 1.05 as Krt/Vurea falls tozero. The eKdt/Vurea of 1.05 corresponds to singlepool Kdt/Vurea values of 1.46 and 1.20 at treat-ment times of 2.0 and 4.0 hours, respectively.

There is emerging evidence that RRF is betterpreserved in patients undergoing HD with theuse of more biocompatible membranes.34

APPENDIX A REFERENCES1. Churchill DN, Taylor DW, Keshaviah PR: Adequacy

of dialysis and nutrition in continuous peritoneal dialysis:Association with clinical outcomes. J Am Soc Nephrol7:198-207, 1996

2. Tattersall JE: Is continuous ambulatory peritoneal di-

Fig II-3. Equivalent total dialysis doses for incre-mental replacement of Kprt/Vurea. Assumptions aremade that the Kr, Kp, and Kd are clinically equivalentclearance items. Another assumption for this particu-lar model is that an equal nPCR, the CAPD steady-state BUN equals the average prehemodialysis BUN.Thus, the intermittent hemodialysis dose can be re-lated to the continuous dialysis (CAPD) by the variouscurves. N � (�) 1, (E) 2, or (■ ) 3 refers to once, twice,or thrice weekly hemodialysis treatments, respec-tively. The vertical axis is the equilibrated (doublepool) delivered and normalized hemodialysis dose.Equilibrated Kt/V is about 0.21 lower than single pooland is necessary to use here because the CAPD steady-state is equilibrated.


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4. Ikizler TA, Greene JH, Wingard RL, Parker RA, HakimRM: Spontaneous dietary protein intake during progression ofchronic renal failure. J Am Soc Nephrol 6:1386-1391, 1995

5. Hakim RM, Lazarus JM: Initiation of dialysis. J AmSoc Nephrol 6:1319-1328, 1995

6. Pollock CA: Protein intake in renal disease. J Am SocNephrol 8:777-783, 1997

7. Teehan BP, Schleifer CR, Brown JM, Sigler MH,Raimondo J: Urea kinetic analysis and clinical outcome onCAPD. A five year longitudinal study. Adv Perit Dial 6:181-185, 1990

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23. Tzamaloukas AH, Murata GH: Body surface area andanthropometric body water in patients on CPD. Perit Dial Int15:284-285, 1995 (letter)

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27. Diaz-Buxo J, Lowrie E, Lew N, Zhang H, Zhu X,Lazarus JM: Associates of mortality among peritoneal dialy-sis patients with special reference to preitoneal transportrates and solute clearance. Am J Kidney Dis 33:523-534,1999

28. Lamiere N, Van Biesen W: The impact of residualrenal function on the adequacy of peritoneal dialysis. PeritDialysis Int 17:S102-S110, 1997 (suppl 2)

29. Popovich RP, Moncrief JW: Kinetic modeling ofperitoneal transport. Contrib Nephrol 17:59-72, 1979

30. Teehan BP, Schleifer CR, Sigler MH, Gilgore GS: Aquantitative approach to the CAPD prescription. Perit DialBull 5:152-156, 1985

31. Keshaviah PR, Nolph KD, Prowant B, Moore H,Ponferrada L, Van Stone J, Twardowski ZJ, Khanna R:Defining adequacy of CAPD with urea kinetics. Adv PeritDial 6:173-177, 1990

32. Gotch FA: Prescription criteria in peritoneal dialysis.Perit Dial Int 14:S83-S87, 1994

33. Eknoyan G, Levey AS, Beck GJ, Agodoa LY, Daugir-das JT, Kusek JW, Levin NW, Schulman G: The hemodialy-sis (HEMO) study: Rationale for selection of interventions.Semin Dial 9:24-33, 1996

34. McCarty JT, Jenson BM, Squillace BS, Williams AW:Improved preservation of residual renal function in chronichemodialysis patients using polysulfone dialyzers. Am JKidney Dis 29:576-583, 1997

APPENDICES S115

Appendix B

The original PD Adequacy Guideline 2 andAppendix B have been replaced by Guideline 27of the Nutrition Guidelines. Members of both thePD Adequacy and the Nutrition Work Groupsdeveloped the updated Guideline. The Guideline

is reproduced as Guideline 2 of the updated PDAdequacy Guidelines without the reference cita-tions which are given in the Nutrition guidelines.Therefore, the reader is encouraged to read theNutrition Guidelines to obtain the references.

Appendix C: Detailed Rationale for Guideline 6

GUIDELINE 6

Assessing Residual Kidney Function (Evidence)

Residual kidney function (RKF), which canprovide a significant component of total soluteand water removal, should be assessed by mea-suring the renal component of Kt/Vurea (Krt/Vurea)and estimating the patient’s glomerular filtrationrate (GFR) by calculating the mean of urea andcreatinine clearance.

Rationale The contribution of RKF to totalsolute and water clearance is significant (30% to50%), especially during the first few years ofdialysis therapy. Assessment of RKF is impor-tant for several reasons. A substantial fraction(30%) of the total renal replacement therapy maybe provided by RKF when a patient begins PD.1

After 2 years of PD, the RKF may still contributeabout 15% of the total Kt/Vurea. Since the RRFcontribution will be added to that of PD, it willbe measured in the same units and for the samesolutes.

Preservation of RKF may be of particularimportance to the effectiveness of long term PDtherapy. There is a progressive decline of RKFover time with both HD and PD. Several studieshave compared the rate of decline of RKF withthe two dialytic modalities2-8 and demonstratedthat RKF is preserved better in patients undergo-ing PD therapies compared to HD. In a study of25 CAPD patients and 25 HD patients, the rate ofdecline of creatinine clearance was significantlyslower over the first 18 months of dialysis in theCAPD patients.2 The PD patients started dialysiswith an uncorrected CCr of 4.4 mL/min, and after18 months it was 4.0 mL/min. In the HD pa-tients, CCr at initiation was 4.3 mL/min, and after18 months it was 1.3 mL/min (P � 0.01 com-pared to PD).

Similar differences were observed in patients

with diabetes.8 In another study comparing theurine output and CCr, the urine output droppedsignificantly in HD patients at the end of 1 yearcompared to 3 years in CAPD patients.3 Themean annual decline of CCr was identical in HDand CAPD for patients with primary glomeru-lopathy. However, in the groups with nephroscle-rosis and tubulointerstitial nephritis, the rate ofdecline of CCr was significantly slower in CAPDcompared to HD patients. In another retrospec-tive study of 4 years duration which compared 55CAPD patients to 57 HD patients, the rate ofdecline in the HD group was twice that of theCAPD group.4 This difference persisted afteradjustment for age, gender, hypertensive status,and the use of ACE inhibitors. Children have abetter preservation of urinary volume, but notGFR, in those receiving PD.7

Despite their limitations, these studies gener-ally demonstrate a slower rate of decline of RKFin patients on PD compared to HD. They alsodemonstrate that the rate of the decline variesfrom patient to patient. The faster rate of declineof RKF in HD is speculated to be due to repeti-tive hypotensive episodes, possibly complementactivation and cytokine release, and the possibil-ity that the more efficient HD may remove GFRstimulatory factors.

Several methods for measuring the CCr compo-nent of RKF are available. These include theuncorrected CCr, a flat percentage of uncorrectedCCr as an estimate of GFR, or the average ofcreatinine and urea clearance also as an estimateof GFR.

While each method has its particular merits,the Work Group recommends using the arith-metic mean of creatinine and urea clearances todetermine the RKF component to CCr and as anestimate of GFR. Therefore, the CCr componentof RKF will subsequently refer to residual renal


CCr, corrected for secretion by taking the arith-metic mean of urea and creatinine clearances.This method was selected for several reasons.First, it was used in some of the major outcomestudies used in establishing these guidelines (seeGuideline 15: Weekly Dose of CAPD). Second,the corrected CCr correlates better with Kt/Vurea

than the uncorrected CCr.9 Third, it makes concep-tual sense because the peritoneal transport ofcreatinine is by diffusion and convection, notsecretion. The correction process addresses this.

The MDRD study derived two equations whichmay approximate GFR,10 one utilizing demo-graphic, serum, and urine variables:

GFR in mL/min per 1.73 m2 � 198

� (serum creatinine concentration in mg/dL)�0.858

� (age)�0.167 � (0.822 if patient is female)

� (1.178 if patient is black)

� (serum urea nitrogen in mg/dL)�0.293

� (urine urea nitrogen in g/day)�0.249

and the other equation using demographic andserum variables only:

GFR in mL/min per 1.73 m2 � 170

� (serum creatinine concentration in mg/dL)�0.999

� (age)�0.176 � (0.762 if patient is female)

� (1.180 if patient is black)

� (serum urea nitrogen in mg/dL)�0.170

� (serum albumin concentration in g/day)�0.318

However, the Work Group recommends usingurea clearance, normalized to total body water,ie, Krt/Vurea, as the key measure to follow seriallyto determine whether urine collections need tocontinue (see Guideline 11: Dialysate and UrineCollections). This is termed the renal Kt/Vurea orKrt/Vurea. This recommendation was made tosimplify the concept of a residual kidney compo-nent to the total renal replacement dose. Kt/Vurea

is believed to be the more valuable measure ofrenal replacement therapy and the Work Groupcarried this thinking through to using Krt/Vurea inboth initiation of dialysis and for following RKFchanges over time.

Krt/Vurea as a measure of RKF is recom-mended because total Kt/Vurea is associated in aclinically important and statistically significantway with patient survival1,11,12 (see Guideline 15:Weekly Dose of CAPD). The peritoneal clear-ance of creatinine is about 80% of the ureaclearance, while at end-stage the kidney clear-ance of creatinine is about 1.5 to 2 times that ofurea. Perhaps as a consequence of this physiolog-ical phenomenon or for other reasons, there is adiscrepancy between total Kt/Vurea and total CCr

normalized to 1.73 m2 BSA (see paragraphsbelow). In the case of discrepancy, Kt/V urea ispreferentially recommended to determine PDadequacy, because it is more predictable andreproducible and is independent of the confound-ing effects of renal secretion of creatinine. Aretrospective study of PD adequacy demon-strated an association between Kt/Vurea and out-comes.13

This emphasis on using Krt/Vurea is not in-tended to detract from the utility of CCr. In termsof validity, total CCr normalized to 1.73 m2 BSAis predictive of patient survival, technique sur-vival, and hospitalization.1 The creatinine genera-tion rate is useful for assessment of nutritionalstatus, in particular, in measuring fat-free, edema-free body mass. Total CCr may also be useful forassessment of compliance.

CCr as an index of PD adequacy is associatedstatistically with both morbidity and mortality1

and correlates with urea clearance.14 Discrepan-cies between the two clearances may be found inapproximately 20% of PD subjects.15,16 The mainreasons for the discrepancies are the presence ofsubstantial RKF, which tends to cause dispropor-tionately high CCr values, and low peritonealsolute transport type, which tends to cause dispro-portionately low CCr values.15,16 CCr values corre-sponding to a weekly Kt/Vurea of 2.0 differ be-tween CAPD subjects with and without RKF(see Fig II-2, referenced previously in AppendixA: Detailed Rationale for Guideline 1). In pa-tients with RKF the mean CCr corresponding to aKt/Vurea of 2.0 weekly is between 60.514 and67.615 L/wk/1.73 m2. In anuric CAPD subjects,the mean CCr corresponding to a Kt/Vurea of 2.0weekly is 52.1 L/wk/1.73 m2.16

In the case of a discrepancy, the Work Grouprecommends the use of Kt/Vurea as an immediate

APPENDICES S117

guide of dialysis adequacy because it directlyrelates to protein metabolism. However, if thereis a discrepancy between CCr and Kt/Vurea, thepatient must be observed closely because ini-tially it may not be clear why the discrepancyexists and the reason may be important. This isdiscussed in Guidelines 1, 7, and 15.

APPENDIX C REFERENCES1. Churchill DN, Taylor DW, Keshaviah PR: Adequacy

of dialysis and nutrition in continuous peritoneal dialysis:Association with clinical outcomes. J Am Soc Nephrol7:198-207, 1996

2. Rottembourg J, Issad B, Gallego JL, Degoulet P, AimeF, Gueffaf B, Legrain M: Evolution of residual renal func-tion in patients undergoing maintenance haemodialysis orcontinuous ambulatory peritoneal dialysis. Proc Eur DialTransplant Assoc 19:397-403, 1982

3. Cancarini GC, Brunori G, Camerini C, Brass S, ManiliL, Maiorca R: Renal function recovery and maintenance ofresidual diuresis in CAPD and hemodialysis. Perit Dial Bull6:77-79, 1986

4. Lysaght MJ, Vonesh EF, Gotch F, Ibels L, Keen M,Lindholm B, Nolph KD, Pollock CA, Prowant B, Farrell PC:The influence of dialysis treatment modality on the declineof remaining renal function. ASAIO Trans 37:598-604, 1996

5. Hallett M, Owen J, Becker G, Stewart J, Farrell PC:Maintenance of residual renal function: CAPD versus HD.Perit Dial Int 12:S46A, 1992 (abstr)

6. Lutes R, Perlmutter J, Holley JL, Bernardini J, PirainoB: Loss of residual renal function in patients on peritonealdialysis. Adv Perit Dial 9:165-168, 1993

7. Feber J, Scharer K, Schaefer F, Mikova M, Janda J:Residual renal function in children on haemodialysis andperitoneal dialysis therapy. Pediatr Nephrol 8:579-583, 1994

8. Rottembourg J: Residual renal function and recoveryof renal function in patients treated by CAPD. Kidney Int43:S106-S110, 1993 (suppl 40)

9. Bhatla B, Moore HL, Nolph KD: Modification ofcreatinine clearance by estimation of residual creatinine andurea clearance in CAPD patients. Adv Perit Dial 11:101-105,1995

10. Levey AS, Bosch J, Breyer LJ, Greene T, Rogers N,Roth D: A more accurate method to estimate glomerularfiltration rate from serum creatinine: A new prediction equa-tion. Ann Intern Med 130:461, 1999


12. Teehan BP, Schleifer CR, Brown JM, Sigler MH,Raimondo J: Urea kinetic analysis and clinical outcome onCAPD. A five year longitudinal study. Adv Perit Dial 6:181-185, 1990

13. Selgas R, Bajo MA, Fernandez-Reyes MJ, Bosque E,Lopez-Revuelta K, Jimenez C, Borrego F, De Alvaro F: Ananalysis of adequacy of dialysis in a selected population onCAPD for over 3 years: The influence of urea and creatininekinetics. Nephrol Dial Transplant 8:1244-1253, 1993

14. Nolph KD, Twardowski ZJ, Keshaviah PR: Weeklyclearances of urea and creatinine on CAPD and NIPD. PeritDial Int 12:298-303, 1992

15. Chen HH, Shetty A, Afthentopoulos IE, OreopoulosDG: Discrepancy between weekly KT/V and weekly creati-nine clearance in patients on CAPD. Adv Perit Dial 11:83-87, 1995

16. Tzamaloukas AH, Murata GH, Malhotra D, Fox L,Goldman RS, Avasthi PS: Creatinine clearance in continu-ous peritoneal dialysis: Dialysis dose required for a minimalacceptable level. Perit Dial Int 16:41-47, 1996

Appendix D: Detailed Rationale for Guideline 8

GUIDELINE 8

Reproducibility of Measurement (Opinion)

Accurate measurement of total Kt/Vurea andtotal creatinine clearance (Ccr) requires collec-tion and analysis of urine, dialysate, and serum ina way that yields reproducible and valid results.Dialysate creatinine concentration must be cor-rected for the presence of glucose in some as-says. Peritonitis precludes reliable measurementof delivered PD dose for up to 1 month. Compli-ance with complete collections is mandatory. Forpatients who void �3 times per day, a 24-hoururine collection is sufficient. For patients whovoid less frequently, a 48-hour collection is rec-ommended. For CAPD patients, the serum sample

can be obtained at any convenient time. ForNIPD patients, the serum sample should be ob-tained at the midpoint of the daytime emptyperiod. For CCPD patients, the serum sampleshould be obtained at the midpoint of the day-time dwell(s).

Rationale To be clinically useful, measure-ment of PD dose must be performed in a validand reproducible fashion. The following factorsinfluence the validity and reliability of Kt/Vurea

and total CCr as measures of PD dose.Dialysate glucose. Dialysate creatinine con-

centration should be corrected for the presenceof glucose, which interferes with some creatininemeasurement methodologies.1 Each facility mustdetermine this by specifically inquiring of its


laboratory whether the creatinine assay used bythat lab is altered by high glucose concentrations.Each laboratory should establish its own correc-tion factor and should reestablish the correctionfactor if the laboratory’s methodology changes.The Work Group does not recommend usingcorrection factors from the literature.

Peritonitis. Peritoneal solute transport in-creases during peritonitis and usually recoverssome time after resolution of peritonitis, with areported recovery time between 3 days2 and 1month.3

Patient compliance with the dialysis prescrip-tion. Following creatinine appearance in dialy-sate and urine longitudinally is an objectivemethod to evaluate the degree of compliance(see Guideline 7: PD Dose Troubleshooting).Clinical tools for evaluating compliance are inthe process of development.4

Variability of residual renal function (RRF).Day-to-day total clearances can vary greatly inPD. The major portion of this variance is causedby changes in measured RKF,5 although creati-nine generation may vary in apparently stablePD patients.6

Completeness of urine collection. To avoidsampling errors, urine should be collected over48 hours in patients who void infrequently (�3times in 24 hours). A 24-hour urine sample canbe used for all other patients. The urine collec-tion should be performed on the same day as thedialysate collection. In children, the urine collec-tion period may be reduced to a minimum of 12hours.

Dialysate and urine collection for PD ad-equacy studies. Two methods of dialysate sam-pling predominate. In the first method, for CAPD,all effluent bags in a 24-hour period are broughtto the center. While this “batch” method is simplein concept, it is difficult to carry out because itmeans transporting all the dialysate bags, whichare heavy and bulky.

The second method is referred to as the “ali-quot” method. In this approach, each bag ofeffluent dialysate is shaken vigorously for a fewseconds, then is emptied into a measuring con-tainer accurate to an error of �50 mL per 2,000mL. The volume for that bag is recorded in mLand the decimal point is moved three places tothe left. The resulting figure is the number of mL

which must be drawn from the dialysate effluentin the measuring container and placed in thelaboratory red top test tube, provided by thedialysis center. For example, if the effluent vol-ume for the CAPD bag is 2,450 mL, moving thedecimal point three places to the left means that2.45 mL of this fluid is put in the test tube (orother small collection container). Each bag forthe 24-hour interval is handled this way. Thealiquots are measured by syringes; usually a5-mL syringe is accurate enough. The aliquotscan be mixed in the same container, because thesampling proportion from each original bag isconstant at 1/1,000. The total effluent is re-corded, and that figure plus the small containerwith all the collected aliquots are brought to thedialysis center. Some dialysate manufacturershave developed special aliquoting exchange bagsthat separate an aliquot as part of the exchange.7

The collection of effluent dialysate from auto-mated PD is conceptually similar to that de-scribed above. The effluent drained via a cycleris quantified automatically by the cycler andgenerally pools in one collection container or, ifin several containers, free mixing is possible.Since the effluent volume is known and thecontainers are allowed to mix freely, a sample ofany reasonable volume (eg, 10 mL) can bebrought to the dialysis unit. If several containersare used with equal filling, an equal volumealiquot from each container can be pooled. Thetotal effluent volume must be known and re-corded. If the effluent bags are not freely mixing,then a sample from each bag is required, as wellas the exact volume of the container from whichthe sample was drawn. One cannot extrapolatefrom one container (bag) to the next.

No matter what method is used for dialysate, acomplete and accurately timed urine collection isnecessary. The urine volume is more easily man-aged since it is much smaller than the dialysatevolume. The longer the collection interval, themore reliable are the collections, assuming pa-tient compliance. A timed collection of 12 to 48hours is recommended, depending on how fre-quently the patient voids. Polyuric patients, par-ticularly children, or patients with a short atten-tion span, may void frequently enough that asupervised 12-hour collection is accurate. As forany urine collection, the bladder should be emp-

APPENDICES S119

tied and the urine discarded moments before thestart of the collection period. Then, momentsbefore the end of the collection period, the pa-tient empties the bladder, and this urine, plus allthat has been collected in the interval, completesthe collection. The patient should try to delay thefinal voiding until just before the interval ends.Three or more bladder voidings generally arenecessary for urine collections. For patients whomake little urine and hence void infrequently,48-hour collections may be more informative.

Serum samples. In CAPD, serum concentra-tions of urea and creatinine are relatively con-stant, and thus blood samples can be drawn atany convenient time for clearance determina-tions. For the asymmetric therapies (NIPD andCCPD), blood concentrations are lowest at theend of the cycling period and highest prior to thenext cycling period. Theoretically, the best timeto draw these blood samples is half way betweenthe lowest and highest times. For NIPD patients,the serum sample should be obtained at themidpoint of the daytime empty period. For CCPDpatients, the serum sample should be obtained at

the midpoint of the daytime dwell. For mostNIPD and CCPD patients, this time point conve-niently occurs in the early afternoon.

APPENDIX D REFERENCES

1. Farrell SC, Bailey MP: Measurement of creatinine inperitoneal dialysis fluid. Ann Clin Biochem 28:624-625,1991

2. Raja RM, Kramer MS, Rosenbaum JL, Bolisay C,Krug M: Contrasting changes in solute transport and ultrafil-tration with peritonitis in CAPD patients. Trans Am SocArtif Intern Organs 27:68-70, 1981

3. Krediet RT, Zuyderhoudt FMJ, Boeschoten EW, AriszL: Alterations in the peritoneal transport of water and solutesduring peritonitis in continous ambulatory peritoneal dialy-sis patients. Eur J Clin Invest 17:43-52, 1987

4. Bernardini J: Predicting compliance in home perito-neal dialysis (PD) patients. ASAIO J 42:102A, 1996 (abstr)

5. Rodby RA, Firanek CA, Cheng YG, Korbet SM:Reproducibility of studies of peritoneal dialysis adequacy.Kidney Int 50:267-271, 1996

6. Johansson A-C, Attman P, Haraldsson B: Creatininegeneration rate and lean body mass: A critical analysis inperitoneal dialysis patients. Kidney Int 51:855-859, 1997

7. Smith L, Folden T, Youngblood B, Panlilio F, Gotch F:Clinical evaluation of a peritoneal dialysis kinetic modelingset. Adv Perit Dial 12:46-48, 1996

Appendix E: Detailed Rationale for Guideline 9

GUIDELINE 9

Estimating Total Body Water and Body SurfaceArea (Opinion)

V (total body water) should be estimated byeither the Watson1 or Hume2 method in adultsusing actual body weight, and by the Mellits-Cheek method3 in children using actual bodyweight.

Watson method1:

For Men: V(liters) � 2.447 � 0.3362*Wt(kg)

� 0.1074*Ht(cm) � 0.09516 � Age (years)

For Women: V � � 2.097 � 0.2466*Wt

� 0.1069 � Ht

Hume method2:

For Men: V � � 14.012934 � 0.296785*Wt

� 0.192786*Ht

For Women: V � � 35.270121

� 0.183809*Wt � 0.344547*Ht

Mellits-Cheek method for children3:

For Boys: V (liters) � � 1.927

� 0.465*Wt(kg) � 0.045*Ht(cm), when Ht

� 132.7 cm

V � � 21.993 � 0.406*Wt

� 0.209*Ht, when height is � 132.7 cm

For Girls: V � 0.076 � 0.507*Wt


V � � 10.313 � 0.252*Wt


Body surface area (BSA) should be estimated byeither the DuBois and DuBois method,4 the Ge-han and George method,5 or the Haycock method6

using actual body weight.


For all formulae, Wt is in kg and Ht is in cm:

DuBois and DuBois method: BSA(m2)

� 0.007184*Wt0.425*Ht0.725

Gehan and George method: BSA(m2)

� 0.0235*Wt0.51456*Ht0.42246

Haycock method: BSA(m2)

� 0.024265*Wt0.5378*Ht0.3964

Rationale The practical methods described inthe literature to estimate V include a fixed frac-tion of body weight (0.60 in males and 0.55 infemales, or 0.58 in all subjects) and anthropomet-ric formulae based on sex, age, height, andweight.1-3 The fixed fraction method is inaccu-rate, as it overestimates total body water even inoverhydrated PD subjects.7 Therefore, the WorkGroup recommends that this method not be used.

Both the Watson1 and Hume2 formulae werederived by comparing anthropometric measure-ments to measurements of body water by indica-tor dilution techniques. An advantage of theseformulae is that they were derived in populationswhich included obese subjects and, therefore,can account for obesity. Estimates from theWatson and Hume formulae are, in general, closeto isotopic body water measurements in PDpatients.7 The error of the estimates based onthese formulae can increase in subjects withabnormalities in body water (hydration), becausesuch subjects were systematically excluded fromthe studies used to derive the formulae.8 Indeed,both the Watson and Hume formulae tend toconsistently underestimate isotopic body waterin both lean and obese PD patients with overhy-dration.7 The formulae are recommended as areasonable approximation with systematic error,but acceptable based on ease of determination. Aproposed correction of the formulae for edemarequires careful assessment of the dry weight.The correction considers actual weight at theedematous state as the sum of two weights: thedry weight plus the weight gain secondary toedema. V is the body water at dry weight ob-tained from the Watson or Hume formulae plus,in its totality, the weight gain secondary toedema.8 The Watson and Hume formulae pro-vide similar estimates of V.9 Both formulae pro-

vide unrealistic estimates of V in subjects whoseheight and/or weight differ greatly from the ordi-nary.9 The Mellits-Cheek formulae were derivedfrom subjects aged 1 month to 34 years for malesand 1 month to 31 years for females. In eachcase, the measurement of total body water wasperformed in normal subjects by the use ofdeuterium oxide distribution with simultaneousmeasurement of weight and height.3

Body surface area is derived from anthropo-metric variables.4-6 While the formulae were de-rived in normal subjects, the influence of clinicalconditions on the variability of the calculationsare much less than that noted for total body watercalculations.

Unfortunately, the relationship between thecalculations for V and BSA is not linear.10 WhenBSA increases linearly as obesity develops, Vincreases exponentially. There are gender differ-ences in these relationships as well. For the sameheight and BSA, males have a larger V thanfemales. Future investigations should apply thesame size indicator normalization factor to bothsolutes.

The Work Group considered the special caseof the malnourished, underweight patient. Se-vere malnutrition is associated with low levels ofRKF in patients who did not increase the dose ofPD to compensate for the loss in renal function.11

This evidence suggests that the loss in kidneyfunction may have caused underdialysis as Kprt/Vurea decreased. Underdialysis then caused ure-mia with anorexia and weight loss, which, inturn, resulted in lower V and higher Kprt/Vurea.Thus, while Kprt/Vurea may be in the “acceptable”range in underweight, malnourished individuals,improved nutrition and weight gain is of para-mount importance in these individuals. If thisaim is fulfilled, V will increase and Kprt/Vurea willdecrease to the previous levels, which were inad-equate. Therefore, it is recommended in suchindividuals to provide a dose of PD which willresult in adequate Kprt/Vurea when they reachtheir desired weight without changing the dialy-sis prescription. For malnourished patients de-fined by SGA or Table II-3 below, provide a PDdose to achieve a weekly Kt/Vurea of 2.0 for thevolume of the patient at desired weight. Thecalculation of the target Kprt/Vurea in malnour-ished CAPD subjects equivalent to a weekly

APPENDICES S121

Kprt/Vurea of 2.0 at desired weight is as follows: IfVactual is body water obtained from the Watson orHume formulae using the actual weight andVdesired is body water obtained by the same formu-lae using the desired weight, then for malnour-ished subjects Vactual � Vdesired. The target CAPDweekly Kprt/Vdesired is 2.0 (for CCPD 2.1 andNIPD 2.2). If Kprt/Vactual � x, then for the CAPDpatient:

(Kprt/Vdesired)/(Kprt/Vactual) � 2.0/x or (1)

2.0*Vdesired/Vactual

� x, and x is the new target Kt/Vurea (2)

Equation 2 can be used to calculate the targetKprt/Vurea in malnourished CAPD subjects. For

example, if Vactual is 35 L and Vdesired is 40 L, thenthe weekly target Kprt/Vactual is 2.0 times 40/35 or2.29. In essence, the target of 2.0 is modifiedupward by a factor of Vdesired/Vactual. The recom-mendation to increase the target Kprt/Vurea inmalnourished PD subjects is based on indirectevidence.

The above water volume estimations are usedin the Kt/Vurea measure. Target Kt/Vurea is modi-fied (Equation 2). The same principle applies ifCCr is used. The normalization of CCr by BSAshould correct weightactual for weightdesired in theformula used to determine BSA. This is furtherdiscussed in Guideline 15: Weekly Dose ofCAPD.

The concept above is intended to deliver a

Table II-3. Median (50th Percentile) Body Weight (kg)

Age Range Males Females

18.0-24.9Frame index �38.4 38.4-41.6 �41.6 �35.2 35.2-38.6 �38.6Median body weight (kg) 68.3 71.5 74.7 55.1 58.1 62.9











Obtained from the NHANES Data as reported by Frishanco.19 Frame Index has no units and is calculated as follows:[Elbow Breadth (mm)/Height (cm)] � 100.

Reprinted with permission.12


dose of PD considered adequate for the patient ata “desired” weight. Defining a “desired” weightcan be subjective, but objective definitions areavailable. One preferable method is that pro-posed by a broad collaborative “glossary” groupwhere the “desired” weight described in thisrationale is the glossary group’s “normal weight,”defined as the median body weight of normalAmericans with the same age, height, sex, andskeletal frame as the patient in question.12 TableII-3 from the glossary details these weight rangesbased on the input parameters of the patient inquestion.

Alterations Caused by Amputation. The an-thropometric formulae for total body water calcu-late that as obesity develops and body weightincreases, V also increases, but body water con-tent (the ratio V/weight) decreases. This is consis-tent with the known fact that water content of fattissue is low. Calculations of V in amputees byuncorrected anthropometric formulae (using theactual postamputation weight and height in thecalculations) distorts the relationship between Vand weight. In this case, body water content isnot consistent with the degree of obesity.13,14 Theanthropometric formulae can be corrected in away that restores the relationship between bodywater content and degree of obesity in threesteps:

Step A: The fraction of body weight lost toamputation (fw) is obtained from a nomogram15

(see Table II-4). The fraction of weight loss (fw)is the percent loss in weight from Table II-4divided by 100. The hypothetical nonamputatedweight at the same body composition would beequal to actual weight/(1 � fw).

Step B: V at the hypothetical nonamputatedweight (Vnon-amputated) is calculated from

the Watson formula. Body water content isVnon-amputated/Weightnon-amputated.

Step C: Actual V is calculated by multiplyingthe actual postamputation weight by Vnon-amputated/Weightnon-amputated. This correction makes the as-sumption that amputation per se will not changebody water content.14

The calculations for body surface area (BSA)in amputees should be also corrected, because ofinconsistent results obtained with the uncor-rected calculation of BSA.16 The correction re-quires also three steps:

Step A: Same as step A in the correction of Vin amputees.

Step B: BSA at the hypothetical nonamputatedweight is calculated by one of the three BSAformulae above.

Step C: The fraction of BSA corresponding tothe amputated limb(s) (fBSA) is obtained fromTable II-4 derived from Herndon. The fraction(fBSA) lost is the percent loss from Table II-4divided by 100. Corrected BSA is BSAnon-amputated

times (1 � fBSA).17

APPENDIX E REFERENCES

1. Watson PE, Watson ID, Batt RD: Total body watervolumes for adult males and females estimated from simpleanthropometric measurements. Am J Clin Nutr 33:27-39,1980

2. Hume R, Weyers E: Relationship between total bodywater and surface area in normal and obese subjects. J ClinPathol 24:234-238, 1971

3. Mellits ED, Cheek DB: The assessment of body waterand fatness from infancy to adulthood. Monographs Soc ResChild Dev, Serial 140 35:12-26, 1970

4. Du Bois D, Du Bois EF: A formula to estimate theapproximate surface area if height and weight be known.Nutrition 5:303-311, 1989

5. Gehan E, George SL: Estimation of human bodysurface area from height and weight. Cancer Chemother RepPart I 54:225-235, 1970

6. Haycock GB, Chir B, Schwartz GJ, Wisotsky DH:Geometric method for measuring body surface area: Aheight-weight formula validated in infants, children, andadults. J Pediatr 93:62-66, 1978

7. Wong KC, Xiong DW, Kerr PG, Borovnicar DJ, StroudDB, Atkins RC, Strauss BJG: Kt/V in CAPD by differentestimations of V. Kidney Int 48:563-569, 1995

8. Tzamaloukas AH: Effect of edema on urea kineticstudies in peritoneal dialysis patients. Perit Dial Int 14:398-401, 1994

9. Tzamaloukas AH, Dombros NV, Murata GH, Nicolo-poulou N, Dimitriadis A, Kakavas J, Malhotra D, AntoniouS, Balaskas EV, Voudiklari S: Fractional urea clearanceestimates using two anthropometric formulas in continuous

Table II-4. Fraction of Weight and BSACorresponding to Amputated Limbs

Body Part Amputated% Loss inWeight14

% of BSAto Subtract16

Foot 1.8 3.5Leg below knee 6.5 10.0Leg above knee 8.0 12.5Leg at hip 18.5 18.0Hand 0.8 2.5Arm at elbow 3.1 6.0Arm at shoulder 6.6 10.0

APPENDICES S123

peritoneal dialysis: Gender, height and body compositiondifferences. Perit Dial Int 16:135-141, 1996

10. Tzamaloukas A, Malhotra D, Murata G: Gender degreeof obesity and discrepancy between urea and creatinine clear-ance in peritoneal dialysis. J Am Soc Nephrol 9:497, 1998

11. Jones MR: Etiology of severe malnutrition: Results of aninternational cross-sectional study in continuous ambulatoryperitoneal dialysis patients. Am J Kidney Dis 23:412-420, 1994

12. Kopple JD, Jones MR, Keshaviah PR, Bergstrom J, Lind-say RM, Moran J, Nolph KD, Teehan BP: A proposed glossaryfor dialysis kinetics. Am J Kidney Dis 26:963-981, 1995

13. Tzamaloukas AH, Saddler MS, Murphy G, Morgan K,Goldman RS, Murata GH, Malhotra D: Volume of distributionand fractional clearance of urea in amputees on continuousambulatory peritoneal dialysis. Perit Dial Int 14:356-361, 1994

14. Tzamaloukas AH, Murata GH: Estimating urea vol-ume in amputees on peritoneal dialysis by modified anthro-pometric formulas. Adv Perit Dial 12:143-146, 1996

15. Hopkins B: Assessment of nutritional status. Nutri-tional Support Dietetics Corte Curriculum. (ed 2). SilverSpring, MD, American Society for Parenteral Nutrition,1993, pp 15-70

16. Tzamaloukas AH, Malhotra D: Creatinine clearancein amputees on CPD. Perit Dial Int 16:426 1996

17. Anonymous: Pre-hospital management, transporta-tion and emergency care, in Herndon DN (ed): Total BurnCare. Philadelphia, PA, Saunders, 1996, pp 36-38

18. US Renal Data Systems: Tthe USRDS Dialysis Mor-bidity and Mortality Study (Wave 1), in National Insti-tutes of Health, National Institute of Diabetes and Digestiveand Kidney Diseases (ed): U.S. Renal Data Systems 1997Annual Data Report. Chapter 4. Bethesda, MD, 1997, pp49-67

19. Frishanco AR: Anthropometric Standards for the As-sessment of Growth and Nutritional Status. Ann Arbor, MI,University of Michigan Press, 1990

Appendix F: Detailed Rationale for Guideline 12

GUIDELINE 12

Assessment of Nutritional Status (Opinion)

Nutritional status of adult PD patients shouldbe assessed on an ongoing basis in associationwith Kt/Vurea and CCr measurements using theProtein equivalent of Nitrogen Appearance (PNA)and Subjective Global Assessment (SGA). Forpediatric PD patients, nutritional status should beassessed using the PNA and other standard nutri-tional assessments (see Guideline 14 of the Clini-cal Practice Guidelines for Peritoneal DialysisAdequacy and the Clinical Practice Guidelinesfor Nutrition in Chronic Renal Failure).

Rationale Although nutritional status de-pends on many nondialysis-related factors, appe-tite suppression, nausea, and vomiting are majorclinical features of inadequate dialysis. There-fore, nutritional status is also an important mea-sure of PD adequacy. Of the available measuresof nutrition, PNA is recommended because itprovides an estimate of protein catabolic rate(PCR) and other protein losses. The SGA isrecommended because it is a clinical assessmentof patient nutritional status and is strongly asso-ciated with patient survival. Both measures arediscussed in detail below.

Protein Equivalent of Nitrogen Appearance(PNA). PNA is a useful tool for monitoring theabsolute level of changes in dietary protein in-take. Nitrogen intake is almost entirely (95%) inthe form of protein. Therefore, total nitrogenexcretion in stable humans multiplied by 6.25

(there are approximately 6.25 grams of proteinper gram of nitrogen) should be a good estimateof protein intake.1 This relationship does nothold true for: individuals in a state of catabolismwhere body cell mass may be contributing tonitrogen excretion; conditions of anabolism wherethe opposite occurs; and inconsistencies in abso-lute or time-averaged blood concentrations ofBUN or creatinine.

In normal humans and in dialysis patients innitrogen balance who have no direct proteinlosses in urine, dialysate or feces, the total dailyexcretion of nitrogen in urine, dialysate, feces,breath, and skin losses is in the form of lowmolecular weight nitrogenous metabolites (suchas urea, creatinine, urate, amino acids, ammonia,and peptides).1

The excretion of nitrogen as low molecularweight metabolites multiplied by 6.25 approxi-mates the amount of nitrogen in ingested protein.This calculation has been termed the proteincatabolic rate (PCR).1,2 PCR actually representsthe net amount of protein catabolism exceedingprotein synthesis required to generate an amountof nitrogen equal to that excreted. The nitrogenin ingested protein enters the body nitrogen pools;nitrogen excreted in urine, feces, breath, skin,and dialysate represents the metabolism of avariety of body substances in these pools, such ascreatine and purine, in addition to body proteins.Thus, although PCR is a reasonable estimate ofprotein intake, not all excreted nitrogen comes


directly from protein. The protein catabolicequivalent of nitrogen excretion is actually a netcatabolic equivalent, rather than an absolute. Itrelates directly to the contribution of proteincatabolism to uremic toxicity.

In patients on hemodialysis, nitrogen balancestudies have been performed to estimate totalnitrogen output or appearance (skin losses wereestimated and breath losses were ignored).2 Therelationship of urea nitrogen appearance to totalnitrogen output was assumed to be fixed and aformula was developed, known as the Borahequation, to calculate the PCR directly from ureanitrogen appearance2:

PCR (g/d) � 6.49*UNA � 0.294*V (1)

where UNA represents the net production orappearance of urea nitrogen in body fluids (anyincrease in body fluid nitrogen concentrationtimes body water volume) and all measurableoutputs in g/d; V is the volume of distribution ofurea in liters. In hemodialysis patients with nodirect protein losses in dialysate or urine, thisPCR also represents an estimate of dietary pro-tein intake and is the protein equivalent of totalnitrogen appearance (PNA).

In dialysis patients with substantial urinary ordialytic protein losses (�0.1 g/kg), the directprotein losses must be added to the PCR to yieldthe true PNA as an estimate of dietary proteinintake.3,4 Thus, in PD:

PNA � PCR � protein losses (2)

Nitrogen balance studies have also been per-formed in PD patients; the measured total nitro-gen output (appearance) included estimates ofskin and fecal nitrogen losses plus measurementof all nitrogen (including protein nitrogen) indialysate and urine.4,5 The average daily dialy-sate protein loss in the CAPD patients was 7.3grams. Urine protein losses were �1 g/24 hours.A formula for the calculation of PNA from UNAwas developed:

PNA (g/d) � 10.76*(0.69*UNA � 1.46) (3)

This calculation incorporates the average dialy-sate protein loss of 7.3 g/d.

Calculations of PNA in PD patients with Equa-tions 2 and 3 have been shown to yield nearlyidentical results.3-5 Also, subtracting protein losses

in dialysate from Equation 3 yields values nearlyidentical to the PCR calculated by Equation 1, asdeveloped in HD patients.4

If daily peritoneal dialysate protein losses ex-ceed 15 grams, PNA calculated from Equation 2will exceed PNA calculated from Equation 3 byapproximately 0.1 g/kg standard body weight.5

High transporters lose more protein into effluentdialysate than other PD patients.7,8 Therefore, inhigh transport patients it is best to measureprotein losses in dialysate directly, and if dialy-sate protein losses exceed 15 g/d (found in �10%of peritonitis-free patients), calculate PNA fromEquation 2.5 For patients who lose large amountsof protein from any nonperitoneal source (eg,nephrotic syndrome), Equation 2 should be used.

Equations 2 and 3 have been validated withnitrogen balance studies only in CAPD and notin other therapies such as NIPD.3-5 However,since CAPD and HD patients have similar PCRvalues (PNA � protein losses) at any givenUNA, the intermittent nature of NIPD wouldseem unlikely to alter the relationships. Further-more, the daily protein losses on NIPD are simi-lar to those of CAPD.9 As more patients anddifferent operating variables were studied, theaccuracy of formulae to predict the nPNA ma-tured. The Bergstrom method is to obtain thenPNA surrogate for dietary protein intake by:

PNA (g/24 hours) � 15.1

� (6.95 � urea nitrogen appearance in g/24h)

� dialystate and urine protein in g/24 hours6

In the absence of direct measurement of urinaryand dialystate protein losses, this less accurateformula may be used:

PNA (g/24 hours) � 20.1

� (7.50 � urea nitrogen appearance in g/24 hr)

When protein losses are high, this second for-mula should not be used. Both formulae willrequire normalization to body mass in kg. TheseBergstrom formulae were preferred in a smallstudy from Italy.10

In summary, the most accurate determinationof PNA in patients undergoing PD uses Equation2, but this requires measurement of UNA anddialysate protein losses. Equation 3 is a suitablesubstitute and requires only measurement of

APPENDICES S125

UNA. However, if dialysate protein exceeds 15g/d (many high transporters may fall into thiscategory) and in all pediatric patients, Equation 2is preferred.

Methods of normalizing PNA are still underdebate. The Work Group recommends normaliza-tion by standard weight, which has been appliedextensively. Standard weight is equal to V/0.58.11

PNA normalized by either standard weight oractual weight tends to be high in malnourished,underweight PD subjects.12 Normalization ofPNA to fat-free, edema-free body mass providesappropriately low nPNA values in underweightindividuals.13 The Work Group recommends thatfat-free, edema-free body mass, estimated fromcreatinine kinetics (see Section II: Measures ofPD Dose) should be used, in addition to standardweight, to normalize PNA in underweight PDsubjects, defined by Table II-3 in Appendix E.Normalizing is important for patient-to-patientcomparisons and to follow PNA measurementsserially in an individual patient whose weightmay change. If weight is stable, normalization isless important in serial measurements for anindividual patient. See Guideline 14 for PNAdiscussion on pediatric patients.

Subjective Global Assessment (SGA). TheSGA is a valid estimate of nutritional status forpatients treated with PD.13 Furthermore, it isassociated with the probability of patient sur-vival.14 The SGA was developed as a clinicalestimate of pre-operative nutritional status.15 Fortwo physicians, the interobserver agreement was72% greater than would have been predicted bychance alone. Validity was based on correlationswith three measures of postoperative hospitalmorbidity (incidence of infection, use of antibiot-ics and length of stay).15 A detailed description ofthe SGA was provided by Detsky in 1987.16

The SGA was originally developed as a clini-cal assessment of preoperative nutritional statusfor patients prior to gastrointestinal surgery.15,16

When applied to CAPD patients,13 validity test-ing reduced the number of items to four (weightloss, anorexia, loss of subcutaneous tissue, andmuscle mass). To increase the ability of the SGAto detect a change in nutritional status, the scor-ing scale was increased from a 3-point to a7-point scale. During the development phase, theSGA was determined by physicians, research

nurses, and nurse clinicians16 but was deter-mined by dialysis nurses and dietitians whenused in the CANUSA study.14

The SGA, as modified for use in CAPD pa-tients,13 uses a 7-point scale14 which any health-care professional can apply following a shorttraining period.

The four items used to assess nutritional statusin CAPD patients are: weight change, anorexia,subcutaneous tissue, and muscle mass.

Weight change is addressed by the question,“What was the patient’s weight change over thepast 6 months?” Ideally, this should be docu-mented by the actual weights, but historical infor-mation from the patient is acceptable. A loss of�10% is severe and 5% to 10% is moderate,while 5% is mild. This is rated subjectively on ascale from 1 to 7, where 1 or 2 is severe malnutri-tion, 3 to 5 is moderate to mild malnutrition, and6 or 7 is mild malnutrition to normal nutritionalstatus. If the weight change was intentional, theweight loss would be given less subjective weightwhile edema might obscure greater weight loss.

Anorexia is addressed by the question, “Hasthe patient’s dietary intake changed?”

Supplemental questions determine whether adecrease in dietary intake is by prescription ordue to decreased appetite. Nausea and vomitingare adverse factors for this item. Again, theinterviewer will rate intake on the 7-point scalewith higher scores indicative of better dietaryintake, better appetite, and the absence of nauseaand vomiting.

Subcutaneous tissue (fat and muscle wasting)can be examined in many areas. A very detailedand illustrated brochure is available from BaxterHealthcare (publication #BRU-008-312-2000).Although the history-taking format is more de-tailed than required, the description of how todetermine muscle wasting and subcutaneous tis-sue is excellent.

Subcutaneous fat can be assessed by examin-ing the fat pads directly below the eyes and bygently pinching the skin above the triceps andbiceps. The fat pads should appear as a slightbulge in a normally nourished person but are“hollow” in a malnourished person. When theskin above the triceps and biceps is gentlypinched, the thickness of the fold between theexaminer’s fingers is indicative of the nutritional


status. The examiner then scores the observa-tions on a 7-point scale.

Muscle mass and wasting can be assessed byexamining the temporalis muscle, the promi-nence of the clavicles, the contour of the shoul-ders (rounded indicates well-nourished; squaredindicates malnutrition), visibility of the scapula,the visibility of the ribs, and interosseous musclemass between the thumb and forefinger, and thequadriceps muscle mass. These are scored on a7-point scale.

The four item scores are then aggregated into aglobal score. The global score is not a simplearithmetic average of the four items. The exam-iner can apply different weights to the items. Forexample, if the physical examination items clearlyindicate severe malnutrition, but the patient indi-cates only a moderate decrease in weight and agood appetite, the examiner might weight thephysical examination items higher than the his-torical items.

In 23 CAPD patients four items were statisti-cally associated with the SGA: weight loss, an-orexia, loss of subcutaneous tissue, and loss ofmuscle mass (muscle wasting).13 Evidence forvalidity was provided by the correlations withserum albumin concentration, bioelectrical im-pedance, anthropometric measurements and nor-malized protein catabolic rate.

Using the SGA as originally described,16 59%of prevalent CAPD patients were well-nour-ished.17 Mild and severe malnutrition was re-ported in 33% and 8% of the patients, respec-tively. In 263 hemodialysis patients and 224CAPD patients18 the SGA covaried with lowvisceral (ie, serum) protein concentrations,midarm muscle circumference (somatic proteinmass), and body fat stores.

In the CANUSA study of peritoneal dialysis,14

weight loss, anorexia, loss of subcutaneous tis-sue, and loss of muscle mass (muscle wasting),as identified above as being statistically associ-ated with the SGA,13 were used to generate theSGA for the CANUSA study. To make the scalemore discriminative, the 3-point scale was ex-panded to a 7-point scale, with 1 and 2 corre-sponding to severe malnutrition, 3 to 5 corre-sponding to mild to moderate malnutrition, and 6to 7 corresponding to mild malnutrition to nor-mal nutritional status. In a multivariate analysis,

a higher SGA was associated with a lower rela-tive risk of death. A one unit increase on the7-point scale was associated with a 25% declinein the relative risk of death (relative risk, 0.75).During the first 6 months of dialysis, the meanSGA increased 0.72 units. There was a statisti-cally significant correlation between the incre-ment in adequacy due to the addition of perito-neal clearance (Kt/Vurea and CCr) to RRF. Overthe next 12 months, there was a small decrease inSGA and this correlated with loss of RRF esti-mated by CCr, but not with Kt/Vurea.19

APPENDIX F REFERENCES

1. Kopple JD, Jones MR, Keshaviah PR, Bergstrom J,Lindsay RM, Moran J, Nolph KD, Teehan BP: A proposedglossary for dialysis kinetics. Am J Kidney Dis 26:963-981,1995

2. Borah MF, Schoenfeld PY, Gotch FA, Sargent JA,Wolfson M, Humphreys MH: Nitrogen balance during inter-mittent dialysis therapy of uremia. Kidney Int 14:491-500,1978

3. Keshaviah PR, Nolph KD: Protein catabolic rate calcu-lations in CAPD patients. ASAIO Trans 37:M400-M402,1991

4. Randerson DH, Chapman GV, Farrell PC: Amino acidand dietary status in CAPD patients, in Atkins RC, FarrellPC, Thompson N (eds): Peritoneal Dialysis. Edinburgh, UK,Churchill Livingston, 1981, pp 179-191

5. Usha K, Moore H, Nolph KD: Protein catabolic rate inCAPD patients: Comparison of different techniques. AdvPerit Dial 12:284-287, 1996

6. Bergstrom J, Heimberger O, Lindholm B: Calculationof protein equivalent of total nitrogen appearance from ureaappearance: which formulas should be used? Perit DialysisInt 18:467-473, 1998

7. Malhotra D, Tzamaloukas AH, Murata GH, Fox L,Goldman RS, Avasthi PS: Serum albumin in continuousperitoneal dialysis: Its predictors and relationship to ureaclearance. Kidney Int 50:1501-1507, 1996

8. Nolph KD, Moore HL, Prowant B, Twardowski ZJ,Khanna R, Gamboa S, Keshaviah P: Continuous ambulatoryperitoneal dialysis with a high flux membrane. ASAIO J904-909, 1993

9. Kathuria P, Goel S, Moore HL, Khanna R, TwardowskiZJ, Nolph KD: Protein losses during CAPD. Perit Dial Int16:S9A, 1996 (abstr)

10. Mandolfo S, Zucchi A, D’Oro LC, Corradi B, Imbas-ciati E: Protein nitrogen appearance in CAPD patients: Whatis the best formula? Nephrol Dial Transplant 11:1592-1596,1996

11. Nolph KD, Moore HL, Prowant B, Meyer M, Twar-dowski ZJ, Khanna R, Ponferrada L, Keshaviah P: Crosssectional assessment of weekly urea and creatinine clear-ances and indices of nutrition in continuous ambulatoryperitoneal dialysis patients. Perit Dial Int 13:178-183, 1993

12. Harty JC, Boulton H, Curwell J, Heelis N, Uttley L,Venning MC, Gokal R: The normalized protein catabolic

APPENDICES S127

rate is a flawed marker of nutrition in CAPD patients.Kidney Int 45:103-109, 1994

13. Enia G, Sicuso C, Alati G, Zoccali C: Subjectiveglobal assessment of nutrition in dialysis patients. NephrolDial Transplant 8:1094-1098, 1993


15. Baker JP, Detsky AS, Wesson DE, Wolman SL,Stewart S, Whitewell J, Langer B, Jeejeebhoy K: Nutritionalassessment. A comparison of clinical judgement and objec-tive measurements. N Engl J Med 306:969-972, 1982

16. Detsky AS, McLaughlin JR, Baker JP, Johnston N,Whittaker S, Mendelson RA, Jeejeebhoy KN: What is sub-jective global assessment of nutritional status? J ParenterEnteral Nutr 11:8-13, 1987

17. Young GA, Kopple JD, Lindholm B, Vonesh EF,DeVecchi A, Scalamogna A, Castelnovo C, Oreopoulos DG,Anderson GH, Bergstrom J, Dichiro J, Gentile D, NissensonA, Sakhrani L, Brownjohn A, Nolph KD, Prowant BF,Algrim CE, Martis L, Serkes KD: Nutritional assessment ofcontinuous ambulatory peritoneal dialysis patients: An inter-national study. Am J Kidney Dis 17:462-471, 1991

18. Cianciaruso B, Brunori G, Kopple JD, Traverso G,Panarello G, Enia G, Strippoli P, De Vecchi A, Querques M,Viglino G, Vonesh E, Maiorca R: Cross-sectional compari-son of malnutrition in continuous ambulatory peritonealdialysis and hemodialysis patients. Am J Kidney Dis 26:475-486, 1995

19. McCusker FM, Teehan BP, Thorpe K, Keshaviah P,Churchill D: How much peritoneal dialysis is required forthe maintenance of a good nutritional state? Kidney Int50:S56-S61, 1996

Appendix G: Detailed Rationale for Guideline 15

GUIDELINE 15

Weekly Dose of CAPD (Evidence)

For CAPD, the delivered PD dose should be atotal Kt/Vurea of at least 2.0 per week and a totalcreatinine clearance (CCr) of at least 60 L/wk/1.73 m2 for high and high-average transporters,and 50 L/wk/1.73 m2 in low and low-averagetransporters.

Rationale The evidence supporting this guide-line is derived from theoretical constructs andcohort studies which use either univariate ormultivariate statistical analyses.

The original description of CAPD1 suggestedthat an anephric 70 kg patient with a total bodywater of 42 L would remain in nitrogen balancewith a daily dialysis prescription of 10 L given asfive 2-L exchanges. Full equilibration of ureabetween plasma and dialysate and 2 L/day of netultrafiltration were assumed. This would producea daily urea clearance of 12 L or a weekly ureaclearance of 84 L. For a patient with a total bodywater of 42 L, this corresponds to a weeklyKt/Vurea of 2.0. Others, using the concept of theDialysis Index, suggested that a similar patientwould require 13.5 L daily of equilibrated draineddialysate to maintain nitrogen balance, and thiswould produce a weekly Kt/Vurea of 2.25.2 Thedifference between these two projections is dueto the higher target protein intake used in thelatter calculation. Using the peak urea concentra-tion hypothesis, a weekly Kt/Vurea of 2.0 is equiva-lent to a single pool hemodialysis Kt/Vurea of 1.3

for patients receiving thrice weekly dialysis.3

These theoretical constructs suggest that a weeklyKt/Vurea of 2.0 to 2.25 would be appropriate.

Validation of these theoretical constructs re-quires clinical study. A series of cohort studiesaddressed this issue.4-8 Initially no relationshipwas found between urea clearance and patientsurvival,6 but a reanalysis, using an anthropomet-ric9 estimate for total body water, found thatpatients with a weekly Kt/Vurea �1.5 had anincreased risk of death compared to patients witha weekly Kt/Vurea �1.5. In another study10 amean weekly Kt/Vurea �1.89 was associated witha decreased risk of death compared to patientswith less dialysis, while yet another4 reportedthat patients surviving for a 12-month follow-uphad a mean weekly Kt/Vurea of 2.0 compared to amean of 1.7 among those who did not survive for12 months. A Belgian group reported that 16patients surviving 5 years on CAPD had a meanweekly Kt/Vurea of 2.0.5 These studies all usedunivariate analysis and therefore did not simulta-neously evaluate the association between otherimportant variables (eg, age, diabetes, cardiovas-cular disease) and patient survival.

Several studies have used multivariate statisti-cal analysis to evaluate the association betweenadequacy of PD and survival while controllingfor other variables.7,8,11,12 In one such study alower serum albumin concentration, increasedage, greater time on dialysis, and lower weeklyKt/Vurea were associated with a decreased prob-ability of patient survival.11 A French group


reported that patients with a weekly Kt/Vurea

�1.7 and a weekly CCr of �50 L/1.73 m2 atinitiation of dialysis had better survival thanthose with lower values at initiation.7 However,these investigators did not evaluate the effect ofchanges in adequacy over time due to loss ofRKF, nor did they attempt to evaluate any asso-ciation of higher weekly Kt/Vurea or CCr withsurvival. An Italian group evaluated the associa-tion between estimates of adequacy and patientsurvival in a cohort of 68 prevalent continuousPD patients followed over 3 years.8 A meanweekly Kt/Vurea of 1.96 was associated withbetter survival than lower values. No furtherbenefit was observed with a Kt/Vurea higher than1.96. Among these patients, a weekly Kt/Vurea

of 1.96 corresponded to a weekly CCr of 58L/1.73 m2.

The Canada-USA (CANUSA) study evaluatedthe association between adequacy of PD andpatient survival, technique survival, and hospital-ization among 680 incident patients (new tostarting PD) treated with continuous PD.12 Adecrease of 0.1 in weekly Kt/Vurea was associatedwith a 5% increase in the relative risk of death,and a decrease of 5 L/1.73 m2/wk in CCr wasassociated with a 7% increase in the risk ofdeath. The risk of technique failure increasedwith decreased creatinine clearance, but was notassociated with Kt/Vurea. Hospitalization in-creased with decreased CCr. Using data derivedfrom the multivariate analysis, the predicted2-year survival associated with a constant weeklyKt/Vurea of 2.1 was 78%. The correspondingweekly CCr was 70 L/1.73 m2.

Thus, there is both a theoretical rationale andconvincing evidence supporting an associationbetween greater clearance of urea and creatinineand better patient survival. There is also evi-dence supporting an association between greaterCCr to longer technique survival and less hospital-ization. In summary, theoretical constructs1-3 sug-gest that the minimum weekly Kt/Vurea should be2.0. Cohort studies using univariate statisticalanalysis support this “target.”4-8,11,12 The CA-NUSA study predicts, among North Americanpatients, a 78% 2-year survival with a weeklyKt/Vurea of 2.1.12

There are no theoretical data to support aspecific CCr target. The CCr which corresponds to

a weekly Kt/Vurea of 2.1 in the CANUSA studywas 70 L/1.73 m2/wk. The Italian group foundthat a weekly Kt/Vurea of 1.96 corresponded to aweekly CCr of 58 L. The CANUSA study in-volved incident patients with significant RKF,while the Italian study evaluated prevalent pa-tients with much less RKF.8 The target of 60L/1.73 m2/wk was selected by the Work Groupbecause it is more relevant to patients with dimin-ished renal function.

Even after controlling for delivered dose, lowand low-average transporters have better patientand technique survival outcomes than do highand high-average transporters.13 In the absenceof adequate residual renal function, low andlow-average transporters may not be able toachieve a CCr of 60 L/wk/1.73 m2 on any reason-able dialysis prescription. However, because ureaclearance is less affected than creatinine clear-ance by transport status, low and low-averagetransporters can achieve a weekly Kt/V of 2.0.Therefore, it seems reasonable to lower the CCr

target in low and low-average transporters with-out jeopardizing the outcomes. These patientsmust be observed closely for evidence of inad-equate dialysis.

There are few data to address the issue ofadequate compared to optimal dialysis. The latteris defined in part as the dialysis dose abovewhich the incremental clinical benefit is notjustified by the social cost to the patient or thefinancial cost to society. Whether or not in-creased weekly Kt/Vurea greater than 2.0 will beassociated with improved clinical outcomes re-quires further study.

The relative importance of RKF compared toperitoneal clearance and the relative importanceof urea compared to CCr are important and inter-related issues. The convention has been to con-sider RKF and peritoneal clearance to be equiva-lent and therefore additive. Some believe thatrenal clearance is more important, but in theabsence of data establishing the magnitude ofthat difference, the assumption of equivalencewas adopted by the Work Group. CCr appearedmore important than urea clearance in the CA-NUSA study.12 The former was associated withpatient survival, technique survival, and hospital-ization, while the latter was associated only withpatient survival. One potential explanation for

APPENDICES S129

this finding is that CCr is more strongly associ-ated with better RKF than was Kt/Vurea. Thisexplanation is based on the assumption that RKFis better than peritoneal clearance, an opinion notyet supported by evidence.

The equivalence of peritoneal and residualkidney clearance is controversial. Current datasuggest inconsistent conclusions. There is a strongsuggestion that protein metabolism is similar inpatients with progressive chronic kidney dis-ease.14 Peritoneal clearance has been shown topredict survival.15,16 However, a large retrospec-tive analysis suggested that peritoneal clearancewas not predictive of survival, while residualkidney clearance was.17 Thus, the Work Grouphas adopted the position that until more defini-tive data are available to direct us, the simplestsolution is to continue to equate residual kidneyand peritoneal clearance. To that end, the preser-vation of kidney clearance is paramount andstrategies to achieve this have recently beendescribed.18

Until evidence to the contrary is available, theWork Group recommends that kidney and perito-neal clearances be considered equivalent. If thereis discordance between achieving the target Kt/Vurea and CCr, the Kt/Vurea should be the immedi-ate determinant of adequacy since it reflectsprotein catabolism. However, the reason for thediscrepancy should be sought and the patientmonitored closely for clinical signs of underdialy-sis.

A special case is the underweight patient,defined in Table II-3, Appendix E. Successfulefforts to restore weight to a normal level in sucha patient will result in a rising V, and conse-quently in a proportionally declining Kprt/Vurea.To provide a weekly Kprt/Vurea of 2.0 at the finalincreased weight, the weekly target Kprt/Vurea

provided during the malnourished state must begreater than 2.0. The Work Group recommendsthat the target Kprt/Vurea should be raised in amalnourished CAPD patient to the level thatwould provide a weekly Kprt/Vurea of 2.0 for thatpatient if he or she was at normal weight. Thatlevel is calculated by multiplying the target of2.0 for CAPD times the ratio of Vdesired/Vactual.This is described in detail in Appendix E: De-tailed Rationale for Guideline 9, and discussed inGuideline 17: PD Dose in Subpopulations. The

same upward target adjustment would be madein CCr. The target CCr should be increased by afactor of BSAdesired/BSAactual.

Clinical judgment suggests that the target dosesof PD for children should meet or exceed theadult standards. However, there are currently nodefinitive outcome data in pediatrics to suggestthat any measure of dialysis adequacy is predic-tive of well-being, morbidity, or mortality. Thereare limited data regarding the real protein needsof children, especially young children, on dialy-sis. It is the opinion of the Work Group that thenutritional requirements per kilogram of bodyweight are higher in children than in adults.Therefore, PD doses in children, and especiallysmall infants who have very high protein intakes,may have to be higher than PD doses in adults.

APPENDIX G REFERENCES

1. Popovich RP, Moncrief JW: Kinetic modeling of peri-toneal transport. Contrib Nephrol 17:59-72, 1979

2. Teehan BP, Schleifer CR, Sigler MH, Gilgore GS: Aquantitative approach to the CAPD prescription. Perit DialBull 5:152-156, 1985

3. Keshaviah PR, Nolph KD, Prowant B, Moore H,Ponferrada L, Van Stone J, Twardowski ZJ, Khanna R:Defining adequacy of CAPD with urea kinetics. Adv PeritDial 6:173-177, 1990

4. De Alvaro F, Bajo MA, Alvarez-Ude F, Vigil A, Mo-lina A, Coronel F, Selgas R: Adequacy of peritoneal dialysis:Does Kt/V have the same predictive value as in HD? Amulticenter study. Adv Perit Dial 8:93-97, 1992

5. Lameire NH, Vanholder R, Veyt D, Lambert M, Rin-goir S: A longitudinal, five year survey of urea kineticparameters in CAPD patients. Kidney Int 42:426-432, 1992

6. Blake PG, Sombolos K, Abraham G, Weissgarten J,Pemberton R, Chu GL, Oreopoulos DG: Lack of correlationbetween urea kinetic indices and clinical outcomes in CAPDpatients. Kidney Int 39:700-706, 1991

7. Genestier S, Hedelin G, Schaffer P, Faller B: Prognos-tic factors in CAPD patients: A retrospective study of a10-year period. Nephrol Dial Transplant 10:1905-1911, 1995

8. Maiorca R, Brunori G, Zubani R, Cancarini GC, Ma-nili L, Camerini C, Movilli E, Pola A, d’Avolio G, Gelatti U:Predictive value of dialysis adequacy and nutritional indicesfor mortality and morbidity in CAPD and HD patients. Alongitudinal study. Nephrol Dial Transplant 10:2295-2305,1995

9. Blake PG, Balaskas E, Blake R, Oreopoulos DG: Ureakinetics has limited relevance in assessing adequacy ofdialysis in CAPD. Adv Perit Dial 8:65-70, 1992

10. Teehan BP, Schleifer CR, Brown J: Urea kineticmodeling is an appropriate assessment of adequacy. SeminDial 5:189-192, 1992

11. Teehan BP, Schleifer CR, Brown JM, Sigler MH,Raimondo J: Urea kinetic analysis and clinical outcome on


CAPD. A five year longitudinal study. Adv Perit Dial 6:181-185, 1990


13. Churchill D, Thorpe K, Nolph K, Keshoviah P, Oreo-poulos P, Page D: Increased peritoneal membrane transportis associated with decreased patient and technique survivalfor continuous peritoneal dialysis patients. J Am Soc Neph-rol 9:1285-1292, 1998

14. Mehrotra R, Saran R, Moore H, Prowant B, KhannaR, Twardowski Z, Nolph K: Toward targets for initiation ofchronic dialysis. Perit Dial Int 17:497-508, 1997

15. Jager KI, Merkus M, Dekker F, Boeschoten E, TijssenJ, Stevens P, Bos WJ, Krediet R: Mortality and technique

failure in patients starting chronic peritoneal dialysis: Re-sults of the Netherlands Cooperative Study on the adequacyof dialysis. Kidney Int 55:1476-1485, 1999

16. Davies S, Phillips L, Russel G: Peritoneal solutetransport predicts survival on CAPD independently of re-sidual renal function. Nephrol Dial Transplant 13;962-968,1998

17. Diaz-Buxo J, Lowrie E, Lew N, Zhang H, Zhu X,Lazarus JM: Associates of mortality among peritoneal dialy-sis patients with special reference to preitoneal transportrates and solute clearance. Am J Kidney Dis 33:523-534,1999

18. Lamiere N, Van Biesen W: The impact of residualrenal function on the adequacy of peritoneal dialysis. PeritDial Int 17:S102-S110, 1997 (suppl 2)

Appendix H: Detailed Rationale for Guideline 19

GUIDELINE 19

Identify and Correct Patient-Related Failure toAchieve Prescribed PD Dose (Opinion)

Potential patient-related causes of failure toachieve prescribed peritoneal dialysis dose shouldbe investigated and corrected. These include:

● Failure to comply with the prescription.● Lack of understanding of the importance of

adherence to the full prescription.● Sampling and collection errors.Rationale It is the opinion of the Work Group

that to increase the likelihood of achieving aprescribed dose of PD, it is necessary to eluci-date the patient-related causes of failure to achievea prescribed dose. Selection of inappropriatecandidates for PD may result in failure to achievea prescribed dose due to medical, technical,and/or psycho-social reasons. The issue of medi-cally appropriate patient selection is dealt with atlength in Section VIII: Suitable Patients for PD.In addition to the medical reasons for selectingpatients for PD or HD discussed in Section VIII,patient compliance is of paramount importanceand should be explored.

Failure to Comply With the Prescription. Pa-tients may decrease the delivered dose of PD inseveral ways. Some of the ways are listed below:

● Skipping exchanges.● Shortened exchange times.● Dialysate dumping: too much flushing result-

ing in too little fill.1

● Delayed dumping: This is achieved by par-

tially draining before the dwell is com-pleted.

● Reduction of total cycler time.● Unscheduled dry days on CCPD.A validated method to measure patient compli-

ance is not currently available. Methods pro-posed for evaluating compliance include monitor-ing for variations in creatinine output in dialysateand urine2 as detailed in Guideline 7: PD DoseTroubleshooting. Evidence for this recommenda-tion is currently not available. The recommenda-tion represents, therefore, the opinion of theWork Group members.

In the absence of a validated method to mea-sure patient compliance, its prevalence in the PDpopulation is not known. Preliminary data fromthe USRDS DMMS Wave II project show that487 CAPD patients self-report full compliancewith 82.8% of their exchanges.3 One exchange/week is missed by 11.5% of patients and 2 to 3exchanges/week are missed by 4.5% of patients,all self-reported. Other estimates vary between5% and 38%.4 Thus, noncompliance is a majorcause of a delivered PD dose being less than thedesired dose and is potentially preventable.

Lack of Understanding of the Importance ofAdherence to the Full Prescription. Medicalliterature about conditions associated with non-compliance in PD is inadequate. The Work Groupreviewed published information on compliancein hemodialysis5-8 and in drug treatment forchronic illness.9-11 The Work Group believes thatsome of the conclusions in this literature may beapplicable to PD. An important conclusion of the

APPENDICES S131

studies on drug compliance is that lack of educa-tion regarding the importance of adherence to thefull prescription partially contributes to compli-ance failure. Compliance with the drug prescrip-tion improves when the patient is convinced thatthe diagnosis is accurate, the reasons for theprescribed treatment are correct, and the pre-scribed treatment is beneficial.11 Some contendthat patients on dialysis are more likely to followthe prescribed treatment if they can be convincedthat adherence to the prescription is in their owninterest.8 By not understanding the significance,importance, value, or relevance of the collectionsor the exchanges, noncompliance could occurwithout patient concern. Therefore, proper educa-tion about the treatment may increase compli-ance in many PD patients. Patients should beeducated that dialysis prescription may changeover time (different modality and/or increase inthe number or volume of exchanges) due to lossof residual renal function (see Guideline 6: As-sessing Residual Renal Function). The method ofeducation should emphasize the expected posi-tive results (improved survival, well-being) ofadherence to the PD prescription, rather than thenegative outcomes (morbidity, mortality) of non-adherence, to prevent the development of exces-sive anxiety, which has adverse effects on com-pliance.

Patient education should be continuousthroughout the course of PD. Patients should betold the results of the repeated clearance measure-ments and should be aware of the target valuesfor Kprt/V and CCr and of the clinical significanceof these clearances. Prevention of noncompli-ance should include monitoring the patient’s psy-chological status. In studies on compliance todrugs, certain psychiatric conditions, such ashostility toward authority, depression and memoryimpairment, financial problems, impaired mobil-ity, and language or ethnic barriers, have beenassociated with poor compliance.11 In addition,complexity of the prescription9 and chronicity ofthe treatment11 increased noncompliance. In thecase of prolonged treatment, repetition of theteaching at 6-month intervals improved compli-ance.11 In studies on compliance in HD, malegender12 and young age13 were predictors of poorcompliance with different aspects of HD prescrip-tion. Preliminary information suggests that a

general negative attitude of the patients predictsnoncompliance in PD.14 Finally, drug compli-ance improves with better education of the pro-viders about compliance issues.10 The WorkGroup thinks that all of these issues are relevantto PD. The psychological profile which is predic-tive of noncompliance and the best method ofcharacterizing this profile should be a subject forresearch in the future. For the present, the WorkGroup’s opinion is that monitoring of patients’psychological status should be aimed at detect-ing conditions associated with increased risk ofnoncompliance, and particularly at detecting anegative patient attitude towards PD. Teachingpatients about their PD prescription should berepeated at intervals of 6 months or less.

Sampling and Collection Errors. Samplingand collection errors committed by patients dur-ing the clearance study preclude accurate mea-surement of clearance. Such errors include:

● Batch method: the patient may not recog-nize the importance of accidentally spilleddialysate.

● Aliquot method: Inaccurate weighing ofdrain volumes which may be the result ofinaccurate scales or misreading. Dispropor-tionate filling of the syringe with dialysate.

● Errors in weighing bags for variable fillvolumes: for example, when (due to costissues) 3-L bags are being used and only 2.5L are exchanged.

● Incomplete urine collections for the RRFdetermination.

Many of these errors can be prevented bycareful patient instruction about the details andsignificance of the clearance procedure.

APPENDIX H REFERENCES

1. Caruana RJ, Smith KL, Hess CP, Perez JC, Cheek PL:Dialysate dumping: A novel cause of inadequate dialysis incontinuous ambulatory peritoneal dialysis (CAPD) patients.Perit Dial Int 9:319-320, 1989

2. Keen M, Lipps B, Gotch F: The measured creatininegeneration rate in CAPD suggests only 78% of prescribeddialysis is delivered. Adv Perit Dial 9:73-75, 1993

3. US Renal Data Systems: the USRDS Dialysis Morbid-ity and Mortality Study (Wave 1), in National Institutes ofHealth, National Institute of Diabetes and Digestive andKidney Diseases (ed): US Renal Data Systems 1997 AnnualData Report. Chapter 4. Bethesda, MD, 1997, pp 49-67

4. Amici G, Viglino G, Virga G, Gandolfo C, Da Rin G,Bocci C, Cavalli PL: Compliance study in peritoneal dialy-


sis using PD Adequest software. Perit Dial Int 16:S176-S178, 1996

5. Wolcott DL, Maida CA, Diamond R, Nissenson AR:Treatment of compliance in end-stage renal disease. Am JNephrol 6:329-338, 1986

6. King K: Noncompliance in the chronic dialysis popula-tion. Dial Transplant 20:67-68, 1991

7. Rocco MV, Burkart J: Prevalence of missed treatmentsand early sign-offs in hemodialysis patients. J Am SocNephrol 4:1178-1183, 1993

8. Lundin AP: Causes of noncompliance in dialysis pa-tients. Dial Transplant 24:174-176, 1995

9. Porter AM: Drug defaulting in a dialysis patients. BMJ1:218-222, 1969

10. Innui TS, Yourtee GL, Williamson JW: Improved

outcomes in hypertension after physician tutorials. A con-trolled trial. Ann Intern Med 84:646-651, 1976

11. Anderson RJ, Kirk LM: Methods for improving pa-tient compliance in chronic disease states. Arch Intern Med142:1673-1675, 1982

12. Everett KD, Sletten C, Carmach C, Brantley PJ,Jones GN, McKnight LT: Predicting noncompliance to fluidrestrictions in hemodialysis patients. Dial Transplant 22:614-622, 1993

13. Cummings KM, Becker MH, Kirscht JP, Levin NW:Psychosocial factors affecting adherence to medical regi-mens in a group of hemodialysis patients. Med Care 20:567-580, 1982

14. Bernardini J: Predicting compliance in home perito-neal dialysis (PD) patients. ASAIO J 42:102A, 1996 (abstr)

APPENDICES S133

XI. Biographical Sketches of the NKF-K/DOQI Peritoneal DialysisAdequacy Work Group Members

The following are brief sketches that describethe professional training and experience, as wellas principal business affiliations of the WorkGroup members. All Work Group members com-pleted a disclosure statement certifying that anypotential conflict of interest would not influencetheir judgment or actions concerning the NKF-K/DOQI.

Thomas A. Golper, MD, FACP (Work GroupChair), is Medical Director of the Medical Spe-cialties Patient Care Center at Vanderbilt Univer-sity Medical Center in Nashville, TN. He stillpractices nephrology and continues to serve asthe Senior Medical Officer of Renal DiseaseManagement, Inc, a disease management com-pany headquartered in Youngstown, Ohio. Dr.Golper has been working to improve patientoutcomes for the past 23 years. He serves as aCQI advisor to industry and has participated inguideline development for the management ofperitonitis since 1986. Dr. Golper has published136 articles and currently directs research ontopics such as peritoneal fluid-drug interactions,peritonitis in PD, and atherosclerotic/thromboticrisk factors in ESRD. Active in many profes-sional societies, he previously served on theBoard of Directors for the Renal PhysiciansAssociation and currently serves on the Board ofDirectors and Executive Committee of the Ameri-can Association of Kidney Patients. Dr. Golperalso serves on the Advisory Board of K/DOQIand on several RPA Committees.

David Churchill, MDCM, FRCPC, FRCP(Edin) (Work Group Vice-Chair), is Professorof Medicine at McMaster University in Hamil-ton, Ontario, Canada. His funded clinical re-search activities have included urolithiasis re-search, polycystic kidney disease, quality of lifein ESRD, economic analysis, erythropoietin inESRD, and adequacy of peritoneal dialysis. He isco-principal investigator of the Canada-USAstudy (CANUSA) on the adequacy of peritonealdialysis. He has over 100 peer-reviewed publica-tions. Dr. Churchill has served on the scientificreview panels for the NIH, Kidney Foundation ofCanada, and the Ontario Ministry of Health, aswell as on advisory committees for erythropoi-etin and dialysis services in Ontario. He has a

cross-appointment in the Department of ClinicalEpidemiology and Biostatistics, with a focus onevidence-based medicine.

Peter Blake, MB, FRCPC, FRCPI,is Direc-tor of Peritoneal Dialysis at the London HealthSciences Centre, London, Ontario, Canada andAssociate Professor of Medicine at the Univer-sity of Western Ontario. Dr. Blake is also Chairof the Canadian Society of Nephrology Work-group of Peritoneal Dialysis and also CourseDirector of the US National Kidney Foundationcourse on Peritoneal Dialysis. His clinical re-search focuses on the areas of adequacy andnutrition in peritoneal dialysis and also in themanagement of chronic kidney failure in thepredialysis phase. He has written or co-authoredmore than 50 publications in the area of dialysis.He is on the editorial board of the Journal of theAmerican Society of Nephrology, Peritoneal Di-alysis International, and Advances in Renal Re-placement Therapy. He is also co-editor of theThird Edition of handbook of Dialysis.

John Burkart, MD, is Associate Professor ofInternal Medicine/Nephrology and Director ofOutpatient Dialysis Services (CAPD and HD)for the Section of Nephrology at Wake ForestUniversity/Bowman Gray School of Medicine inWinston-Salem, North Carolina. Dr. Burkart hasbeen an active clinical nephrologist for 11 yearsand manages a large nephrology and dialysispractice. He currently cares for 70 end-stagerenal disease patients and participates in a grouppractice serving more than 250 dialysis patients.He serves as a consultant to industry and hasactively participated in clinical trials and educa-tional workshops. Dr. Burkart has written orco-authored more than 90 publications, and iscurrently involved in research related to ad-equacy of peritoneal dialysis, improving out-comes on peritoneal dialysis, and alternativeosmotic agents for peritoneal fluid. He is a co-investigator in the Hemodialysis Study and serveson the editorial boards of Peritoneal DialysisInternational and Advancement of Renal Replace-ment Therapy. Dr Burkart reported an affiliationwith Baxter Healthcare.

Dinesh K. Chatoth, MBBS, is Assistant Pro-fessor of Medicine at the University of Arkansas


for Medical Sciences and Medical Director ofDialysis Services for the John L. McClellanVeterans Affairs Medical Center in Little Rock,Arkansas. Dr. Chatoth received the JD ChastainResearch Award in 1998 from the National Kid-ney Foundation of Arkansas. His main researchinterests are related to cardiovascular disease inperitoneal dialysis, pre-ESRD education and in-cremental dialysis, and sustained low efficiencydialysis in acute renal failure.

Catherine Firanek, RN, CNN, MBA, isGlobal Senior Clinical Marketing Manager forBaxter Healthcare Corporation’s Renal Divisionwhich develops, manufactures and markets hemo-dialysis and peritoneal dialysis products and ser-vices. She currently focuses on establishing clini-cal educational programs and marketing activitiesrelated to dialysis therapy development aroundthe world. For the past 18 years, Ms. Firanek hasbeen involved with peritoneal dialysis programestablishment, patient care, research and educa-tional development at Rush-Presbyterian St.Luke’s Medical Center/Circle Medical Manage-ment in Chicago, IL. Both locally and nationally,Ms. Firanek has been actively involved with theNational Kidney Foundation serving in severalpositions related to nursing educational develop-ment, board of directors and now as co-editor ofthe joint council quarterly publication and CNNTcouncil member at a national level. She was amember of the DOQI PD Adequacy workgroupestablished in 1993. She has served in advisoryand research roles related to industry and haspublished numerous articles in areas of perito-neal dialysis including urban population experi-ence, peritonitis incidence and adequacy.

Denis Geary, MB, MRCP(UK), FRCPC, isAssociate Professor, Department of Pediatrics, atthe University of Toronto, and Chief of Nephrol-ogy at the Hospital for Sick Children in Toronto,Canada. Dr. Geary’s clinical training took placein the United States, United Kingdom, and Ire-land. He has practiced as a staff physician inpediatric nephrology for 15 years. Dr. Geary’spublications involve the subjects of dialysis, andthe growth and development of children withchronic kidney disease.

Frank Gotch, MD, is a consultant to theRenal Research Institute in New York and isAssociate Professor of Medicine at UCSF. Dr.

Gotch has worked in clinical dialysis and dialy-sis research , particularly quantification of therapy,for 30 years. He chaired the NIH Hemodialyzerevaluation Study Group which sets standards fordialyzer performance in 1972 and the NationalNIH conference on Adequacy of Hemodialysisin 1975. He served on the planning committeeand as kinetic consultant to the National Cooper-ative Dialysis Study and serves on the SteeringCommittee of the current HEMO study and wasCo-Principal Investigator of a Cooperative studyof Randomized Peritoneal Dialysis Prescriptionsand Clinical Outcome. He has over 100 publica-tions and provides consultation in dialysis kinet-ics and dialysis systems development to industry.His current research interests are primarily con-cerned with modeling dialysis technology.

Alan S. Kliger, MD, FACP, is Clinical Profes-sor of Medicine at Yale University School ofMedicine and Director of the New Haven CAPD.He currently chairs the ESRD Network of NewEngland, the Quality Improvement Committeeof the Forum of ESRD Networks, and the Qual-ity Patient Care Committee of the Renal Physi-cians Association. Dr. Kliger also serves on theNational Kidney Foundation’s K/DOQI SupportGroup.

Stephen M. Korbet, MD, is Professor ofMedicine at Rush Medical College and AssociateDirector of the Section of Nephrology at Rush-Presbyterian-St. Luke’s Medical Center in Chi-cago Illinois. He also serves as Medical Directorof Circle Medical Management Dialysis Facility.Dr. Korbet is currently a member of the Interna-tional Society of Peritoneal Dialysis Committeeon Education and Standards and Baxter’s Interna-tional Ad Hoc Committee on Ultrafiltration Man-agement in Peritoneal Dialysis. Active in re-search, Dr. Korbet’s interests include nephroticsyndrome, focal segmental glomerulosclerosis,and peritoneal dialysis. He has served on theeditorial board of the American Journal of Kid-ney Disease, and currently serves on the editorialboards of the Journal of Nephrology, and Perito-neal Dialysis International.

Antonios Tzamaloukas, MD, FACP,is Chiefof the Renal Section of the New Mexico VAHealth Care Center and Professor of Medicine atthe University of New Mexico School of Medi-cine. Dr. Tzamaloukas has been on the faculty of

THE NKF-K/DOQI PERITONEAL DIALYSIS ADEQUACY WORK GROUP MEMBERS S135

the University of New Mexico for 25 years. Hehas had a major interest in peritoneal dialysis forthe past 15 years. He has more than 230 scientificpublications and is a member of the editorialboard of the International Journal of ArtificialOrgans, Peritoneal Dialysis International, Kid-ney International, and American Journal of Kid-ney Diseases. He is active in several professionalsocieties. His main research interest is in ad-equacy and nutrition of dialysis patients.

Bradley Warady, MD, is Chief of Nephrol-ogy and Director of Dialysis and Transplantationat The Children’s Mercy Hospital, and Professorof Pediatrics at the University of Missouri –Kansas City School of Medicine. Dr. Warady’sclinical and research focus is end-stage renal

disease, with particular emphasis on peritonealdialysis. He established the Pediatric PeritonealDialysis Study Consortium and currently co-directs research projects on a number of topicsincluding: growth hormone usage in pediatricdialysis patients; peritoneal dialysis adequacy inchildren; and intravenous iron therapy in pediat-ric patients receiving hemodialysis. He co-editedthe book “CAPD/CCPD in Children” and haspublished more than 150 articles. Dr. Waradycurrently serves on the executive committees ofthe American Society of Pediatric Nephrologyand the Nephrology section of the AmericanAcademy of Pediatrics. Dr. Warady also sits onthe Editorial Board for the Advances of RenalReplacement Therapy.


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