R E V I E W P A P E R

How Does Volume Status Affect BNP and Troponin Levels asMarkers of Cardiovascular Status in Peritoneal Dialysis?

T he 2 major hurdles in the manage-ment of end-stage renal disease

(ESRD) patients are cardiovascularcomplications and clinical assessment ofvolume status. Left ventricular (LV)hypertrophy and LV dysfunction deter-mined by echocardiography are frequentcardiac alterations in ESRD and areindependent risk factors for mortality.1

These alterations result from conditionssuch as chronic pressure overload fromincreased systolic blood pressure (BP)and volume overload due to overhydra-tion and arteriovenous shunts in hemod-ialysis (HD).2 Another major challengefaced by nephrologists caring for ESRDpatients is the clinical assessment of vol-ume. Most peritoneal dialysis (PD)treatments incorporate a prescription forfluid removal targeted to the patient’sdry weight, which is clinically estimated.Clinical assessment of dry weight isinexact because of the difficulty in deter-mining the actual hydration status of anindividual patient.3,4 Chronic fluid over-load, which is frequently found in PDpatients, is associated with poor BP con-trol, LV hypertrophy, and cardiac dys-function, all of which are independentpredictors of cardiovascular mortality.3–6

None of the existing techniques areaccurate for assessment of dry weight.Therefore, objective tools for estimatingvolume status are necessary. Biomarkerssuch as brain natriuretic peptide (BNP)and troponin are routinely used in theassessment of LV dysfunction and myo-cardial necrosis in nondialysis popula-tions. BNP is already known to predictvolume overload and mortality in HDpatients but such an association is notwell established in PD patients.7–10

Therefore, the objective of this reviewis 2-fold. First, review the role of BNPand troponin as prognostic markers in

PD patients. Second, examine if eitherof these markers can be used as anobjective tool to estimate clinical vol-ume status in patients on PD.

Role of BNP in PDBNP is a peptide hormone that isreleased primarily by the ventricularmyocytes in response to myocyte stretchsuch as increased cardiac filling pres-sure.11 It is synthesized as an inactiveprohormone (108 amino acid pro-BNP)and is cleaved into the biologicallyactive fragment (32 amino acid c-BNP)and the N-terminal pro-B-type natri-uretic peptide (76 amino acid NT-pro-BNP), and both are measurable inplasma or serum.12–14 Compared withBNP, NT-pro-BNP has the advantage

of having a longer plasma half-life andlower biologic variation.13 There isample evidence that BNP and NT-pro-BNP are useful in diagnosing and pre-dicting prognosis in heart failure.15–22

Furthermore, in patients who are treatedfor acutely decompensated heart failure,BNP concentration declines in parallelwith fall in pulmonary capillary wedgepressure during a period of 24 hours,23

suggesting that BNP mirrors changes influid status and allows monitoring thera-peutic responses in heart failure. Studieshave shown that cardiac natriureticpeptide levels are frequently raised inHD patients compared to patients withnormal renal function even in theabsence of acute coronary syndrome.24

The high plasma concentration of BNP

Cardiac biomarkers such as brain natriuretic peptide, amino-terminal pro-B-type natri-uretic peptide (NT-proBNP), and cardiac troponin provide information on cardiovascularmorbidity and mortality in patients with normal renal function. In a considerable numberof chronic hemodialysis patients, both biomarkers—NT-proBNP and troponin—are ele-vated despite the absence of cardiac ischemia. The elevation of cardiac biomarkers inchronic hemodialysis patients is of prognostic value with respect to cardiovascular mor-bidity and mortality. Furthermore, they can serve as tools for volume assessment for opti-mization of the fluid management aspect of dialysis. However, the association of boththese markers in peritoneal dialysis is not clear. Therefore, the authors reviewed theliterature to examine the role of these markers in peritoneal dialysis patients both asprognostic indicators as well as tools for volume assessment. Congest Heart Fail.2009;15:240–244. �2009 Wiley Periodicals, Inc.

Rajeev Garg, MD;1 Avneet Singh, MD;2 Azam Khaja, MD;1

Alpert Martin, MD;1 Kul Aggarwal, MD1

From the Division of Cardiovascular Medicine, University of Missouri–Columbia,One Hospital Drive, Columbia, MO;1 and the Division of Internal Medicine,NSLIJ–Albert Einstein School of Medicine at Long Island Jewish Medical Center,New Hyde Park, NY2

Address for correspondence:Rajeev Garg, MD, Division of Cardiovascular Medicine, University of Missouri–Columbia, Hospital Drive, Columbia, MO-65202E-mail: rajeevgarg@sbcglobal.netManuscript received December 15, 2008; revised March 24, 2009;accepted April 3, 2009

doi: 10.1111/j.1751-7133.2009.00094.x

cardiac biomarkers in peritoneal dialysis september • october 2009240

in dialysis patients is thought to be mul-tifactorial secondary to extracellular vol-ume expansion, concomitant heartdisease, and reduced renal clearance.24,25

BNP is eliminated from plasma mainlythrough natriuretic peptide receptorsand degraded by neutral endopeptidasesin addition to being excreted via glo-merular filtration.

Similar to HD, Obineche and collea-gues26 confirmed that elevated levels ofBNP, NT-pro-BNP occurred in PDpatients and that levels of these peptideswere not altered by PD.

Zoccali and colleagues27 showed forthe first time in uremic patients on bothHD and PD that plasma concentrationof cardiac peptides is determined mainlyby LV myocardial index (LVMI) andLV ejection fraction (LVEF) and thatBNP is useful in identifying patientswith LV hypertrophy, or for excludingsystolic dysfunction. Also, BNP is a sig-nificant predictor of survival, indepen-dent of LV mass and LVEF in thesedialysis patients.28 However, a study byTaskapan and colleagues29 involvingpatients on HD and PD for longer than2 months, failed to show any significant

association with BNP and LVMI andLVEF in patients on dialysis for<36 months (Table I). Conversely,Nakatani and colleagues30 reported apositive correlation with LVMI and anegative correlation with LVEF inpatients on both continuous ambulatoryPD (CAPD) and HD >36 months.This discrepancy in the value of BNP asa marker could be due to the fact that,in chronic dialysis patients, intracardiacdistension might be less associated withcardiac problems within 3 years. How-ever, both studies reported that plasmaBNP concentration was significantlylower in CAPD patients compared toHD patients (143 pg ⁄mL vs 467 pg ⁄mL)29,30 and the lower levels of BNPin CAPD patients suggests that car-diac load in CAPD patients may belower than that of HD patients due tostable hemodynamic conditions, lowerincidence of systemic hypertension,higher urine output and slower rate ofultrafiltration with PD.30 Despite thelower levels of BNP in PD, it remainsinconclusive whether PD or HD isassociated with better volume and BPcontrol.

The role of NT-pro-BNP as a prog-nostic marker was evaluated in a pro-spective study of Chinese ESRDpatients on CAPD for at least 3 months.This study found that NT-pro-BNP pre-dicts cardiovascular congestion, overallmortality, cardiovascular death, andevents in chronic PD patients over a3 year follow-up. Thus, NT-pro-BNPmay serve as a useful composite biomar-ker of LV hypertrophy and LV dysfunc-tion, residual renal function, andextracellular volume expansion inchronic PD patients.31 However, otherstudies have highlighted a limited rolefor BNP in volume assessment in PDpatients. Plasma BNP levels are knownto decrease significantly after an HD ses-sion, implying that volume overload isan important stimulus for BNP secre-tion32 and hence, BNP levels have beensuggested to be a useful tool for volumeassessment in HD patients. Such anassociation in patients on PD with BNPhas been equivocal. A study done byGranja and colleagues33 failed to showpositive association between clinicalvolume assessment and BNP levels andthoracic fluid content measured by

Table I. BNP Levels and Correlation With Cardiac Parameters in PD

STUDYTUDY BIOMARKERIOMARKER

CORRELATIONORRELATION WITHITH

CARDIACARDIAC

PARAMETERS ANDARAMETERS AND

VOLUMEOLUME STATUS INTATUS IN

PDCORRELATION ASORRELATION AS TOOL FOROOL FOR

VOLUMEOLUME ASSESSMENT INSSESSMENT IN PD

Taskapanet al.29

N=19

BNP: mean values ofBNP in PD patients=143.1�165.2 pg ⁄ mL

No correlation with LVMIor LVEF

Not studied

Nakataniet al.30

N=32

Mean values of BNP in PD patientswithout heart disease=62.1�60.6pg ⁄ mL

› BNP correlates with ›LVMI and fl LVEF

Not studied

Wang et al.31

N=230NT-pro-BNP median value in this studywas 5698 pg ⁄ mL

› NT-pro-BNP levelscorrelated with ›LVMI and fl LVEF

Value more than 11,250 pg ⁄ mL stronglyassociated with volume overload in PDpatients

Granja et al.35

N=51BNP Not studied Mean levels of BNP in euvolemic

patients=477.4 pg ⁄ mL andhypervolemic patients=665.2 pg ⁄ mL.Correlation with clinical assessment of fluidstatus was not statistically significant (P=.48)

Lee et al.34

N=32Mean NT-pro-BNP levels in thisstudy=3924 pg ⁄ mL

Elevated levelscorrelate with ›LVMI and fl LVEF

Poor correlation with volume status

Bavbek et al.35

N=62Mean BNP levels in APD and CAPDpatients (253.23 pg ⁄ mLa vs 109.42pg ⁄ mL,b respectively)

BNP level andLVMI was higherin patients onAPD vs CAPD

Not studied

Abbreviations: APD, automated peritoneal dialysis; BNP, brain natriuretic peptide; CAPD, continuous ambulatory peritoneal dialysis; LVEF,left ventricular ejection fraction; LVMI, left ventricular mass index; PD, peritoneal dialysis. aAPD. bCAPD.

cardiac biomarkers in peritoneal dialysis september • october 2009 241

means of cardiac bioimpedance inchronic PD patients. Similarly, Lee andcolleagues34 also found no correlationbetween NT-pro-BNP levels and extracellular water (ECW) content in PDpatients leading them to conclude thatNT-pro-BNP is an inadequate volumeassessment tool. In agreement with priorstudies on BNP, Lee’s study foundhigher levels of serum NT-pro-BNP inpatients with CAPD compared to nor-mal subjects and a strong correlationwith LVMI and LVEF. One explanationfor the poor association of NT-pro-BNPwith ECW could be that CAPDpatients do not experience rapid volumechanges compared to HD patients; thehigher NT-pro-BNP levels in CAPDpatients compared to healthy volunteerscould be in response to chronic vol-ume overload causing cardiac myocytestretch over an extended period of time.

The limited usefulness of cardiacnatriuretic peptides in assessing volumestatus is also supported by an earlierstudy by Mallamaci and colleagues28

who found that the role of BNP indetermining dry weight in dialysispatients is limited.

Bavbek and colleagues35 comparedtreatment with automated PD (APD)with CAPD and found that the formeris associated with higher plasma BNPlevels and LVMI. This was thought tobe the result of chronic fluid retentioncaused by lower ultrafiltration in APDpatients.

Role of Troponin in PDCardiac troponins T and I (cTnT andcTnI) are subunits of the cardiac

actin–myosin complex, which leakinto the circulation during myocardialdamage, and their detection is used asa sensitive and specific marker ofmyocardial cell necrosis and a predic-tor of adverse outcome in the generalpopulation with unstable coronaryartery disease.36 cTnT is frequentlyincreased in ESRD patients withoutevidence of acute myocardial ische-mia37,38 and is associated with anincrease in all-cause mortality andcardiovascular death.39–44 Several rea-sons have been given for the elevatedlevels of troponin T in ESRDpatients: retention of proteolytic degra-dation products of troponin T whichcan be detected by the cTnT assay,effect of renal clearance, result ofsmall areas of clinically silent myocar-dial necrosis, and LV hypertrophy.Similarly, elevated levels of troponinT over baseline have been found inpatients of PD in the absence of overtmyocardial injury, ie acute coronarysyndrome.42,45 Two prospective studiesby Duman and colleagues andLowbeer and colleagues found thatelevated baseline serum cTnT signifi-cantly predicted total and cardiovas-cular mortality in clinically stableCAPD patients, however, both thesestudies were limited by small samplesize (Table II).42,45 In addition, boththe studies found that cTnI andcreatine kinase MB mass had noprognostic value in patients on PD.However, the Netherlands Coopera-tive Study on the Adequacy of Dialy-sis showed that although cTnTpredicts mortality, it has limited added

predictive value over other clinicalrisk factors (age, renal function, BP)in a mixed cohort of HD and PDpatients.46 This finding is in contrastto the recent study by Wang andcolleagues that troponin T has addedpredictive value over other clinical,biochemical, and echocardiographicmeasures in chronic PD without acutemyocardial ischemia for all-cause mor-tality and cardiovascular death andevents. This study has the largestnumber of PD patients to date andsupplements their previous observationthat cTnT adds significant value toechocardiography in identifying PDpatients at risk of cardiovascularcongestion.47 Most of these studies arein agreement that cTnT levels docorrelate with LV hypertrophy andLVMI in ESRD patients withoutacute myocardial ischemia.40,42

ConclusionsIn summary, the data suggest thatboth BNP and troponin are elevatedin patients with PD and correlatewell with LVEF and LVMI. There-fore, these markers appear to be use-ful in evaluating LV hypertrophy andLV dysfunction in CAPD patientsand their elevated levels indepen-dently identify a subset of patients athigher risk of adverse events includ-ing risk of developing vascular con-gestion in the future. However, thestudies done so far indicate thatserum BNP and NT-pro-BNP have alimited role in volume assessment inCAPD patients; troponin does notappear to be useful in monitoring

Table II. Troponin Levels and Correlation With Cardiac Parameters in Peritoneal Dialysis

STUDYTUDY BIOMARKERIOMARKER

CORRELATIONORRELATION BETWEENETWEEN TROPONINROPONIN LEVELS ANDEVELS AND

TOTALOTAL MORTALITY INORTALITY IN PERITONEALERITONEAL DIALYSISIALYSIS PATIENTSATIENTS

Havekes et al.46

N=265Troponin T >0.10 ng ⁄ mL Correlated with increased total mortality (HR=3.4)

Duman et al.42

N=65Troponin T �0.035 ng ⁄ mLa Correlated with increased total mortality with OR=8.94 (95% CI, 2.23–35.88)

Wang et al.47

N=238Troponin T >0.075 ng ⁄ mLb Correlated with increased total mortality with HR=4.12 (95% CI, 1.29–13.17)

Lowbeer et al.45 N=26 Troponin T >0.04 ng ⁄ mL Correlated with increased total mortality with P<.01

Abbreviations: CI, confidence interval; HR, hazard ratio; OR, odds ratio. aAlso correlates with left ventricular myocardial index. bCutoff0.075 ng ⁄ mL had a sensitivity and specificity of 76% (95% CI, 64%–85%) and 71% (63%–78%), respectively, in predicting mortality andhad a positive and negative predictive value of 52% and 88%, respectively, for mortality.

cardiac biomarkers in peritoneal dialysis september • october 2009242

fluid status in these patients. How-ever, the limitation in most of theabove studies is the small samplesize and isolated measurements ofserum biomarkers rather than serialmeasurements over a period of time.Therefore, clinicians should be cau-

tioned against overzealous interpreta-tion of these data. Future effortsshould be directed to explore new bi-omarkers and efficacy of implantedmonitoring devices with remotecommunication capabilities such asmeasuring thoracic impedance and

pulmonary artery pressure as tools forassessing volume status.

Acknowledgment: Our sincere grati-tude to Dr Mary Dohrman forproofreading this manuscript.

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