Download - Introduction to Nephrology
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Introduction to NephrologyJENNIFER SMITH, FNP-S
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ObjectivesProvide an overview of basic renal anatomy and physiology
Discuss the growing epidemic of chronic kidney disease due to increased incidence of obesity, hypertension, and diabetes
Define the stages of chronic kidney diseases and discuss associated complications such as: anemia of chronic kidney disease, secondary hyperparathyroidism, hypertension, cardiovascular disease, hyperkalemia, hyperphostphatemia, and bone disease
Discuss management of chronic kidney disease
Discuss other common kidney disorders that may lead to end-stage renal disease
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The KidneyLocation- relatively high under lower ribs in the retroperitoneal space
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Anatomy and PhysiologyAverage size of adult kidney is 12x6x3 cm
Size variations can occur with age, gender, BMI, pregnancy, kidney disease, and co-morbid conditions
Right kidney smaller
Right kidney lower than left kidney
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Renal Anatomy
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Structure of KidneyCortex-the outer layer of the kidney comprising the glomeruli, most of the proximal tubules, and some of the distal tubulesMedulla-formed by 7-9 cone shape pyramids which extend into the renal pelvisRenal Pelvis-flat funnel-like tube continuous with ureter as it leaves the hilusCalyces- subdivided into major and minor calycesMajor calyces- 2 or 3 branches off of renal pelvisMinor calyces- cup-shaped areas that enclose the papillae of the pyramids. Continuously collect urine draining from papillae, emptying it into the renal pelvis (Greenburg et al, 2009)
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The Nephron Functional unit of kidney Consisting of glomerulus and long tubuleApproximately 1 million nephrons in each kidneyFilters plasma->reabsorption and secretion->forms filtrate free of protein->regulates the filtrate to maintain fluid volume, electrolytes, and pH
(Greenburg et al, 2009)
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The NephronGlomerulus- tuft of capillaries surrounded by Bowman’s capsule. Together form the renal corpuscle.
Tubules- segmented into proximal tubule, loop of Henle, distal tubule, and collecting tubules
•Tubular Transport:
Proximal Tubule- active reabsorption of sodium
Loop of Henle and distal tubule- concentration or dilution of urine
Collecting Tubules- run through medullary pyramids (give them their striped appearance)
(Greenburg et al, 2009)
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The Nephron
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Blood and Nerve SupplyRenal arteries: branch off of the aorta then further divide to form: segmental arteries:
1. Lobular arteries
2. Interlobar arteries
3. Arcuate arteries
4. Interlobular arteriesMore than ¼ of the cardiac output is delivered to the kidneys each minute (1200ml/min)More than 90% of blood entering kidney perfuses the cortex
(Greenburg et al, 2009)
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Blood and Nerve SupplyRenal Veins- trace pathway of arterial blood supply in reverseEmpty into the inferior vena cavaLeft renal vein is about 2x longer in order to extend to IVC in its position to right of vertebral columnRenal Plexus-network of autonomic nerve fibers and ganglia. Supplied by sympathetic fibers from thoracic and lumbar splanchnic nervesSympathetic fibers- vasomotor fibers that control renal blood flow by adjusting arteriolar diameters
(Greenburg et al, 2009)
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Functions of KidneyMaintenance of body fluids composition (fluid volume, osmolarity, electrolyte, and acid/base balance.Excretion of metabolic end products and foreign substances (i.e. urea, toxins, drugs).Production/secretion of enzymes and hormones
(Greenburg et al, 2009)
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Functions of KidneyRenal Hormones and Enzymes
Renin- produced in juxtaglomerular apparatus. Catalyzes production of angiotensin which is important for sodium balance and blood pressure regulationErythropoietin- stimulates maturation of RBC’s in bone marrow1,25-Dihydroxyvitamin D3- most active form of Vitamin D3, steroid hormone that helps the body regulate calcium/phosphorus balance
(Greenburg et al, 2009)
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Functions of Kidney Alterations in body fluid composition and fluid volume can impact:Cardiac Output and Blood Pressure- dependent on optimal plasma volumeEnzyme Function- most function best in narrow range of pH and ion concentrationsCell Membrane Potential- depends on potassium concentrationsMembrane excitability- depends on calcium ion concentrations
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Evaluation of Renal FunctionGlomerular Filtration Rate (GFR)
Serum Creatinine, Blood Urea Nitrogen
MAU/CR ratio
30-300 mg/dl microalbuminemia
>/= 300mg/dl- macroalbuminemia
24 hour urine collection
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Glomerular Filtration Rate (GFR)GFR- amount of fluid filtered from blood into glomerular capsule each minuteGFR- 180 L/dayGFR controlled by:Auto-regulation (tubuloglomerular feedback)Neural regulationHormonal regulation- renal aldosterone angiotensin system
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ScreeningDM- largest single cause of CKD in the U.S.
Initial screening 5 years after diagnosis of Type I DM
AT DIAGNOSIS of type II DM
Annually thereafter
HTN
Family history of CKD
Autoimmune disorders
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Screening MethodsChemistries-renal panel, include albumin and MGUrinalysisMicroalbumin/Cr ratioImaging studies 24 hour urine
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Abnormalities on Imaging Studies
Renal cysts-often incidental findings and usually benign. Ultrasound is preferred method to differentiate between cystic and solid lesions. (If complex cyst or indeterminate lesions follow up with MRI)
Nephrolithiasis- non-contrast CT is gold-standard
Hydronephrosis
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Chronic Kidney DiseaseCKD is defined as:Kidney damage for 3 months or longer to include either structural or functional abnormalities
With or without a decrease in GFR (as seen by pathology abnormalities, markers of kidney damage in blood or urine, or abnormalities on imaging studies).GFR of less than 60 ml/min for at least 3 months
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Prevalence31 million in U.S. (16% of population) and rising
1 in 10 adults have some level of CKD
Majority of people with CKD are in Stage 1-3
Incidence is increasing rapidly in those >65
ESRD expected to reach 2.2 million by 2030
ESRD males > females
Most people with CKD die before they are diagnoses, primarily of cardiovascular complications
African Americans are 4 times more likely to develop CKD than Caucasians.
(Domino, 2013)
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Risk FactorsHypertension
DM
Autoimmune diseases (vasculitis, connective tissue disorder)
Congenital anomalies
Family history of CKD or transplant
Kidney stones
Frequent urinary tract infections
Exposure to certain drugs (i.e. NSAID)
Cardiovascular disease
Acute Kidney Injury
Systemic infections
Low income/education
Minority populations
Obesity
Smoking
Age > 60 years
Race
Neoplasm
Urinary Tract Obstruction
Hyperlipidemia
(Domino, 2013)
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CKD Staging
(Domino, 2013)
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Clinical Findings of CKD by StageStage I and
II
• Asymptomatic, BUN/CR slightly elevated or normal, acid-base, fluid, and electrolyte balance is maintained through compensation of remaining nephrons
Stage III
• Usually asymptomatic, BUN/CR increased. Erythropoietin decreased and PTH levels are increased
Stage IV
• Patient may have anemia, acidosis, hypocalcemia, hyperphosphatemia, and hyperkalemia
Stage V
• Fatigue, dysgeusia, anorexia, nausea, pruritus, asterixis, uremic breath
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Associated ComplicationsHTN
Anemia
Secondary Hyperparathyroidism (SHPT)
Hyperkalemia
Cardiovascular complications
Bone disease
(Greenburg et al, 2009)
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HypertensionCan be cause or effect
Inappropriate sodium reabsorption leading to increased fluid volume is primary cause of HTN in CKD
RAAS stimulation
Renal Artery Stenosis
Vascular Calcifications
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Managing HTN in CKDGoal is BP < 130/80 mm/HgMany patients will require multiple drug classifications to control BP due to increased vascular resistance and increased fluid volumeUncontrolled HTN is key risk for progression of CKDAn increase in BP of 20/10mmHg doubles risk for cardiovascular disease
(Greenburg et al, 2009)
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Pharmacologic Management HTN in CKDACE/ARB
“Reno protective”
Lowers intra-glomerular pressure and reduces proteinuria, slowing the progression of CKD
May see initial increase in sCr (less than 30% that returns to baseline within 2 months if acceptable)
Monitor K level
Contraindicated in renal artery stenosis, uncontrolled hyperkalemia, pregnancy, history of angioedema
Not unusual to see patients with CKD on several different classifications of medications
(Collins, 2012)
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Pharmacologic Management HTNCalcium Channel Blocker:
Dihydropyrodines-Amlodipine, Valsaartan
Increase intraglomerular pressure causing worsening of proteinuria if not used in combination with a ACE/ARB
Non-Dihydropyrodines (Diltiazem, Verapamil)
If failing on ACE/ARB therapy, have been shown to reduce proteinuria
Vasodilators (Hydralazine, Isosorbide)
May be useful in patients with known renal artery stenosis
(Collins, 2012)
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Pharmacology ContinuedDiuretics
Diuretic resistance may be due to high sodium diet
Loop Diuretics
Best dosed BID for CKD III or higher
May take second dose 6 hours after 1st dose
Monitor serum K+ levels, may need replacement
Thiazide Diuretics
Effective in patients with GFR>30
Monitor uric acid level as may cause gout
Monitor serum K+ levels
(Collins, 2009)
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DiureticsMost CKD patients require diureticsEnhances antihypertensive therapyReduces tubular sodium reabsorption which in turn increases sodium excretion and lowers ECF volume, lowering BPChoice of diuretic depends on CKD stage, volume of fluid overload, and other individual patient factorsUse potassium sparing diuretics with caution if GFR is less than 30, or if concomitant use of ACEI/ARBDon’t decrease diuretics due to increase BUN/Cr. BUN/Cr will fluctuate with fluid volumeDon’t treat the lab, treat the patient!
(Collins, 2009)
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CKD in PregnancyRenal function in CKD may deteriorate during pregnancy
CR >1.5 and hypertension are major risk factors of worsening renal function
Increased risk of premature labor, preeclampsia, and/or fetal loss
ACE inhibitors and ARBs are contraindicated
Use diuretics with caution
(Domino, 2009)
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Parathyroid Gland
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Secondary Hyperparathyroidism (SHPT)The parathyroid glands main function is to control calcium within the blood and bonesParathyroid glands atrophy due to constant stimuli in CKD (either hypocalcemia or hyperphosphatemia).Atrophied glands secrete PTH, causing serum levels to risePTH stimulates conversion of active Vitamin D to increase calcium absorption from the GI tractOver time, elevated PTH leads to bone disease, vascular and soft tissue calcifications, decreased quality of life, amputations, and increased mortality
(Greenberg et al, 2009)
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PTH goal based on Stage of CKD
(National Kidney Foundation, 2010)
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SHPTMonitoring
Intact PTH levels
Ca and Phosphorus levels
Vitamin D 1,25 level
Treatment
Oral Calcitriol, Zemplar, Hectoral, Sensipar
May need Vitamin D replacement
Treat hyperphosphatemia- if you control phosphorus you will control the parathyroid
May need parathyroidextomy
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HyperphosphatemiaIncreases cardiovascular risk factors
Calcifications develop may result in bone deformities and amputations
High levels of phosphorous cause Calcium to be pulled from bone
Osteoporosis
Bone pain
Fractures
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Hyperphosphatemia
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Treatment for Hyperphosphatemia
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Cardiovascular Complications in CKDPatients with CKD more likely to die from CVD
Survival rate of MI patients with CKD are 53% compared to 36%
Vascular calcifications common in patients with hyperphosphatemia and SHPT
Cardio-renal syndrome
Patients with CKD should have annual EKG,
stress test on file
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HyperkalemiaDecreased Renal Excretion
Acute or chronic renal failure
Aldosterone deficiency (frequently associated with diabetic nephropathy, chronic interstitial nephritis, or obstructive uropathy)
Adrenal Insufficiency (Addison’s disease)
Kidney diseased that impair distal tubule function (Sickle cell, Systemic Lupus Erythematosus)
Abnormal Potassium Distribution
Insulin deficiency
B-Blockers
Metabolic and Respiratory Acidosis
Abnormal Potassium Release from Cells
Rhabdomyolysis
Tumor lysis syndrome
(Greenburg et al, 2009)
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Treatment Goals to Slow Progression of CKDControl blood pressure <130/80 or <140/80 in renal artery stenosis
Low NA diet
ACE/ARB therapy
Diuretics
Nondihydropyridine Calcium Channel Blockers
Optimize control of DM (HGA1C <7.5)
Control dyslipidemia LDL goal <100
Restrict dietary protein
Low phosphorous diet
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Prescribing Considerations in CKDDose adjust medications based on GFR (Metformin, Allopurinol, many antibiotics, etc)
Avoid use of nephrotoxic drugs (NSAIDS, contrast dye, Bactrim)
When treating DM with CKD less insulin may be required due to decreased gluconeogenesis
Best to avoid 1st generation sulfonylureas as they have increased risk for hypoglycemia due to decreased renal clearance
Second generation sulfonylureas are preferred (Glipizide)
As always start low and go slow!
(Greenburg et al, 2009)
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Drug-Induced HyperkalemiaBlock Sodium Channel in the Distal Nephron
Potassium-sparing diuretics: amiloride, triamterene
Antibiotics: trimethoprim, pentamidine
Block Aldosterone Production
ACE inhibitors
ARBs
NSAIDS and COX-2 inhibitors
Heparin
Tacrolimus
Block Na+, K+-ATPase Activity in the Distal Nephron
Cyclosporine
Potassium Release from Injured Cells
Drug-induced rhabdomyolysis (lovastatin, cocaine)
Drug induced tumor lysis syndrome(chemotherapy agents in leukemia's, high-grade lymphomas)
Depolarizing paralytic agents (succinylcholine)
Block Aldosterone Receptor
Spironolactone
Eplerenone
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NSAID’sMajor cause of CKD
Block Aldosterone Production
Widespread use of these drugs are leading to increased cases of NSAID-induced nephropathy
Not a problem if no renal impairment
Avoid in CKD and transplant patients
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Diabetic NephropathyAbout 35% of patients with DM (Type I and Type II) will develop nephropathy after about 25 to 30 years
Approximately 45% of dialysis patients have diabetic nephropathy as cause of ESRD
However many type II patients die from CV disease before they reach ESRD
May not be able to tell patient has kidney disease based on GFR
Need to have a micro albumin urine test to determine level of proteinuria
Need to be on ACE/ARB for renal protection
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Renal Artery StenosisClassic findings:
•Uncontrolled HTN despite multiple medications
Causes:
Usually atherosclerosis
Fibro muscular dysplasia
Diagnosis:
Nuclear renal scan, renal arteriogram, MRA, or Doppler ultrasound
Treatment:
Angioplasty or surgery
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Obstructive UropathyObstruction can occur anywhere along urinary tract causing hydonephrosis
Renal calculi
BPH
Colon, cervical, or uterine cancer
Neurogenic bladder
Can be unilateral or bilateral
Treatment
Resolve obstruction- may need stents
Treat BPH
Foley catheter or nephrostomy tubes
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Autosomal Dominant Polycystic Kidney DiseaseMost common inherited kidney disease
Affects 1 in 1000 people
Systemic disease causing kidney, liver, pancreas, thyroid, and subarachnoid cysts and intracranial aneurysm
Clinical hallmark sign is gradual and massive cystic enlargement of kidneys resulting in kidney failure
May be present in childhood with symptoms usually beginning in middle age
Symptoms can include abdominal pain, hematuria, nocturia, flank pain, and fatigue
Diagnosis usually made by ultrasound
Presence of enlarged kidneys with multiple cysts required for diagnosis
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ADPKD
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ADPKD
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Hepatorenal Type I
Usually rapid decline in kidney function
sCr may double in 2 weeks
Occurs with acute hepatitis, bacterial infections, major surgery, or massive GI bleed
Type II
Moderate steady decline in GFR
Cirrhosis causes decrease in NA and water excretion, decreased renal perfusion and GFR
Decreased ability to excrete NA leads to ascites
Presence of ascites represents marked impairment or renal sodium handling
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Cardio-Renal1. Abrupt worsening of cardiac function leads to AKI
2. Chronic abnormalities in cardiac function causes progression of CKD
3. Abrupt worsening of renal function causes acute cardiac dysfunction (heart failure, arrhythmia, or ischemia)
4. CKD contributes to decreased cardiac function resulting in hypertrophy and increased risk of CVD
5. A systemic condition results in both cardiac and renal dysfuction
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Aging and Renal FunctionNatural decline in GFR is 8ml/min for every decade after 40 despite normal creatinine
Renal blood flow declines by 10% per decade
Renal mass decreased from 400g to 300g by age 90
All the above accelerated by: HTN, DM, lead exposure, smoking, atherosclerotic vascular disease, and male gender
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Acute Kidney InjuryIncidence increasing with the number of hospitalizations with AKI diagnosis rose from 3,942 in 1996 to 23,052 in 2008
5% to 30% of hospital ICU admissions
25% of people develop while in the hospital
50% of cases are iatrogenic
Pre-renal- response to hypoperfusion->volume depetion, sepsis, heart failure, cirrhosis
Intra-renal- conditions that affect parenchyma->acute tubular necrosis, acute interstitial nephritis, nephrotoxic medications
Post-renal-obstruction of urinary outflow->BPH, renal calculi
(Domino, 2013)
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Nephrotic SyndromeClinical syndrome characterized by massive proteinuria (>3g/24hrs)
Associated with many types of kidney diseases such as minimal change disease, membranous glomerulopathy, diabetes, and amyloidosis
Hypoalbuminemia
Edema
Hyperlipidemia
Lipiduria
May have fatigue, weight gain, anorexia, foamy urine
Treatment involves addressing underlying cause and complications
May need a kidney biopsy
May require long-term immunosuppressant therapy
(Domino, 2013)
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End-Stage Renal Disease (ESRD)Cardiovascular disorders are leading cause of death for ESRD patients
More than 50% of dialysis patients die from cardiovascular complications
Risk of CV death is 50% higher in this population if patient also has DM
Screen patients annually for CV disease with electrocardiogram, stress test
Refer to cardiologist
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Signs and Symptoms of ESRDHead-headaches, fatigue, and difficulty thinking
Mouth- food may taste bad or like metal, foul smelling breath (like urine)
Lungs-dyspnea caused by fluid or anemia
Stomach- loss of appetite, nausea and vomiting
Bladder- less or no urine. Some people still make urine but it is just fluid no waste products are removed
Hands and feet- swelling
Skin-build up of uremic wastes causes itching
Blood vessels- high blood pressure failing kidneys can no longer keep pressure under control
(Greenburg, 2009)
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HemodialysisDone through a vascular access (fistula, graft, or permacath)
Usually requires four hour sessions three days a week
Special considerations
•Some antibiotics require dose adjustment/timing adjustment to avoid removal of medication
through dialysis
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Peritoneal DialysisAdvantages
Convenient done at home
Daily treatments more closely match natural renal functions
Patients have less fluid/dietary restrictions
Disadvantages
High Risk for peritonitis
Requires compliance with aseptic technique
Patients with history of multiple abdominal surgeries or hernia may not be candidates
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Renal TransplantEvaluation process can start when GFR is <20
Many options are available such living relative, non-related living, and cadaver
Requires extensive workup to be placed on list
Compliance
Requires immunosuppressant therapy
Caution when prescribing/adjusting transplant patient’s medication
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Burden of ESRDEconomic costs
Total Medicare costs for ESRD care in 2005 were $19.3 billion
Decreased quality of life
Increased morbidity and mortality
Complications associated with dialysis
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ReferralElectrolyte abnormalities
Persistent proteinuria
Uncontrolled HTN
Elevated serum CR/decreased GFR –guidelines CR 1.5 female, 2.0 male
Patient with known CKD that are likely to progress
Don’t wait to refer to nephrologist when the patient needs dialysis
Patients need to have dialysis access, education, and preparation
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CollaborationCKD requires collaboration and coordination among many health care providers
CKD stages I-III usually managed by PCP
Nephrologist usually consulted when CKD III or other kidney disorder
Dietician
Cardiologist
Vascular Surgeons
Endocrinologist
Social workers
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Educational ResourcesNational Kidney Foundation www.kidney.org
American Nephrology Nurse’s Association http://ww.annanurse.org
Internet School of Nephrology http://www.Ukidney.com
International Society of Nephrology http://www.theisn.org
American Society of Nephrology http://www.asn-online.org/
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Questions The number one cause of death in patients with ESRD: A. Complications from DM B. Septicemia D. Cardiovascular Disease E. Cancer The functions of the kidney are: A. Production and secretion of enzymes and hormones B. Excretion of metabolic end products and foreign substances C. Maintenance of body fluid composition D. Both A & B E. All of the above The best antibiotic choice for a 69 y/o female with a urinary tract infection A. Cipro 250mg BID B. Bactrim DS 1 tablet BID C. Do not provide antibiotics wait for urine culture
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References Claudio, R., Haapio, M., House, A., Anavekar, N., & Bellomi, R. (2008, November). Cardiorenal
syndrome. Journal of American College of Cardiology, 52(19), 1527-1539.
Collins, T. (2012). Twelve things hospitalists need to know about nephrology. The Hospitalist.
Retrieved February 7, 2014 from http://the-hospitalist.org/details/article/3782901/12
Things Hospitalists Need to Know About Nephrology.html
Deja Review Internal Medicine (2011). Mobasser, S., McGraw Hill Medical, New York
Dunphy, L., Winland Brown, J., Porter, B., & Thomas, D. (2011). Primary Care: The art and science of advanced practice nursing. 3rd Edition.
Philadelphia: F.A. Davis. ISBN 978-0-8036-2255-5.
Domino, F. (2013). Griffith’s 5 Minute Clinical Consult. 19th Ed. Lippincott Williams & Wilkins.
Fibromuscular Dysplasia (n.d.). Retrieved February 7, 2014 from http://www.mayoclinic.com/
health/fibromuscular-dysplasia/DSO1101.
Greenburg, A., Cheung, A.K., Coffman, T.M., Falk, R. J., Jennette, J.C. (2009). Primer on kidney diseases. (5th ed.), Philadelphia, Saunders Elsevier
National Kidney Foundation (2010). Nephrology essentials: chronic kidney disease. Retrieved
February 8,2014 from http://www.kidney.org/professionals/CAP/nephEssentials.cfm
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References National Kidney Foundation (2012). Clinical Practice Guidelines for Chronic Kidney Disease
Evaluation, Classification, and Stratification.
National Kidney and Urologic Diseases Information Clearinghouse (2012). Retrieved February
10, 2014 from http://www.nih.gov/kudiseases/pubs/kustats/#top
Niels-Peter, B., Farhat, A., Syed, R., Biyabani, Q., Masood, A., Imtiaz, R.(2012) Ultrasonographic
renal size in individuals without known renal disease. Journal of Pakistan Medical Association.