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Acute and Chronic Renal Failure Courtney Bunevich, DO December 19, 2007 Acute Renal Failure Rapid decline in the GFR over days to weeks Serum Cr increases by >0.5 mg/dL GFR <10mL/min, or <25% of normal Definitions Anuria: No urine output Oliguria: Urine output <400-500 mL/d Azotemia: Increase in Serum Cr and BUN May be prerenal, renal, or postrenal Does not require any clinical findings Chronic Renal Insufficiency Deterioration over months to years GFR 10-20 mL/min, or 20-50% of normal ESRD: GFR <5% of normal ARF: Signs and Symptoms Hyperkalemia Nausea/Vomiting HTN Pulmonary edema Ascites Asterixis Encephalopathy Causes of ARF in Hospitalized Patients 45% ATN Ischemia, 21% Prerenal CHF, Nephrotoxins volume depletion, sepsis 10% Urinary obstruction 4% Glomerulonephritis or vasculitis 2% AIN 1% Atheroemboli ARF: Focused History Nausea? Vomiting? Diarrhea? Hx of heart disease, liver disease, previous renal disease, kidney stones, BPH? Any recent illnesses? Any edema, change in urination? Any new medications? Any recent radiology studies? Rashes? Physical Exam Volume Status Mucus membranes, orthostatics Cardiovascular JVD, rubs Pulmonary Decreased breath sounds Rales Rash (Allergic interstitial nephritis) Large prostate Extremities (Skin turgor, Edema) Workup for ARF BMP or RFP Urine Urine electrolytes and Urine Cr to calculate FeNa Urine eosinophils Urine sediment: casts, cells, protein Uosm Kidney U/S to rule out hydronephrosis FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr) FeNa <1% PRERENAL ATN (unusual) Urine Na < 20 because functioning tubules reabsorb lots of filtered sodium Postischemic disease: most of UOP comes from few normal nephrons, which handle sodium appropriately ATN + chronic prerenal disease (cirrhosis, CHF) Glomerular or vascular injury Despite glomerular or vascular injury, pt may still have wellpreserved tubular function and be able to concentrate Na FeNa FeNa 1%-2% Prerenal-sometimes ATN-sometimes AIN will have a higher FeNa due to tubular damage FeNa >2% ATN Damaged tubules cannot reabsorb sodium Calculating FeNa after Patient Has Recieved Lasix Caution with calculating FeNa if pt has gotten loop diuretics in past 24-48 h Loop diuretics cause natriuresis that raises U Na-even if the patient is prerenal So if FeNa>1%, you do not know if this is because patient is euvolemic or because lasix increased the U Na So, helpful if FeNa still <1%, but not if FeNa >1% Prerenal ARF Hyaline casts can be seen in normal pts NOT an abnormal finding UA in prerenal ARF is normal Prerenal: causes 21% of ARF in hospitalized patients Reversible Prevent ATN with volume replacement Fluid boluses or continuous IVF Monitor Uop Prerenal causes Intravascular volume depletion Hemorrhage Vomiting, diarrhea “Third spacing” Diuretics Reduced Cardiac output Cardiogenic shock, CHF, Tamponade Systemic vasodilation Sepsis Anaphylaxis, Antihypertensive drugs Renal vasoconstriction Hepatorenal syndrome Intrinsic ARF 1. 2. 3. 4. Tubular (ATN) Interstitial (AIN) Glomerular (Glomerulonephritis) Vascular You evaluate a 57yo man with oliguria and rapidly increasing BUN and Serum Cr A. B. C. D. ATN Acute glomerulonephritis Acute interstitial nephritis Nephrotic Syndrome ATN Muddy brown granular casts (last slide) Renal tubular epithelial cell casts (below) More ATN •Broad casts (form in dilated, damaged tubules) ATN Causes Hypotension Relative low BP May occur immediately after low BP episode or up to 7 days later Post-op Ischemia Post-aortic clamping, post-CABG Crystal precipitation Myoglobinuria Contrast Dye ARF usually 1-2 days after IV contrast load Aminoglycosides ATN Treatment Remove any offending agent IVF Try Lasix if a euvolemic patient is not having adequate urine output Dialysis Most patients return to baseline Serum Cr in 7 to 21 days ATN Cr Prerenal increases at increases 0.3-0.5 /day slower than 0.3 /day U Na, UNa>40 UNa<20 FeNa FeNa >2% FeNa<1% UA epithelial Normal cells, granular casts Response Cr will not Cr to volume improve improves much with IVF Which UA is most compatible with contrast-induced ATN? A. B. C. D. Spec gravity 1.012, 20-30 RBC, 15-20 WBC, positive for eosinophils Spec gravity 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eosinophils Spec gravity 1.012, 5-10 RBC, 25-50 WBC, many bacteria, occasional fine granular casts, no eosinophils Spec gravity 1.020, 10-20 RBC, 2-4 WBC, 1-3 RBC casts, no eosinophils ATN B. Spec gravity 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eosinophils Dilute urine: failure to concentrate urine No RBC casts or WBC casts in ATN Eosinophils classically in AIN or renal atheroemboli, but nonspecific WBC Casts Cells in the cast have nuclei (unlike RBC casts) Pathognomonic for Acute Interstitial Nephritis Acute Interstitial Nephritis 70% Drug hypersensitivity 15% Infection 30% Antibiotics: PCN, Cephalosporins, Cipro Sulfa drugs NSAIDs Allopurinol Strep, Legionella, CMV 8% Idiopathic 6% Autoimmune Diseases Sarcoid, Tubulointerstitial nephritis AIN from Drugs Renal damage is NOT dose-dependent May take weeks after initial exposure to drug Signs and Symtpoms Up to 18 months to get AIN from NSAIDS But only 3-5 days to develop AIN after second exposure to drug Fever (27%) Serum Eosinophilia (23%) Maculopapular rash (15%) Labs Bland sediment or WBCs, RBCs, non-nephrotic proteinuria WBC Casts are pathognomonic Urine eosinophils on Wright’s or Hansel’s Stain Also see urine eosinophils in RPGN and renal atheroemboli AIN Management Remove offending agent Most patients recover full kidney function in 1 year Poor prognostic factors ARF > 3 weeks Advanced age at onset You evaluate a 32yo woman with HTN, oliguria, and rapidly increasing Cr, BUN. You spin her urine: A. B. C. D. ATN Acute glomerulonephritis Acute interstitial nephritis Nephrotic Syndrome Acute Glomerulonephritis RBC casts: cells have no nuclei Casts in urine: think INTRINSIC renal disease If she has Lupus with recent viral prodrome, think Rapidly Progressive Glomerulonephritis (RPGN) If she had a sore throat 10 days ago, think Postinfectious Proliferative Glomerulonephritis Glomerular Disease Hematuria: dysmorphic RBCs RBC casts Lipiduria: increased glomerular permeability Proteinuria: may be in nephrotic range Fever, rash, arthralgias, pulmonary symptoms Elevated ESR, low complement levels Rapidly Progressive Glomerulonephritis Type 1: Anti-GBM disease Type 2: Immune complex Type 3: Pauci-immune Necrotizing glomerulonephritis Often ANCA-positive and associated with vasculitis Can present with viral-like prodrome IgA nephropathy Postinfectious glomerulonephritis Lupus nephritis Mixed cryoglobulinemia Myalgias, arthralgias, back pain, fever, malaise Kidney biopsy : Extensive cellular crescents with or without immune complexes Can develop ESRD in days to weeks Treat with glucocorticoids and cyclophosphamide Postinfectious Proliferative Glomerulonephritis Usually after strep infection of upper respiratory tract or skin after a 8-14 day latent period Can also occur in subacute bacterial endocarditis, visceral abscesses, osteomyelitis, bacterial sepsis Hematuria, hypertension, edema, proteinuria Positive antistreptolysin O titer (90% upper respiratory and 50% skin) Treatment is supportive Screen family members with throat culture and treat with antibiotics if necessary A 19yo woman with Breast Cancer s/p chemo in the ER has weakness, fever, rash. WBC=15.4, Hct 24, Cr 2.9, LDH 600, CK 600. UA=3+ protein, 3+blood, 20 RBC. What next test do you order? What’s her likely diagnosis? A. B. C. D. E. Nephrotic Syndrome ATN Acute Glomerulonephritis Thrombotic Thromboctyopenic Purpura Rhabdomyolysis TTP Order blood smear to rule out TTP TTP associated with malignancy and chemotherapy TTP may mimic Glomerulonephritis on UA (RBCs, WBCs) Thrombocytopenia and anemia not consistent with nephrotic or nephritic syndrome Need CK in the thousands to cause ARF Microvascular ARF TTP/HUS HELLP syndrome Platelets form thrombi and deposit in kidneys leading to glomerular capillary occlusion or thrombosis Plasma exchange, steroids, IVIG, and splenectomy are possible treatments Macrovascular ARF Aortic Aneurysm Renal artery dissection or thrombosis Renal vein thrombus Atheroembolic disease New onset or accelerated HTN? Abdominal bruits, reduced femoral pulses? Vascular disease? Embolic source? Your 68yo male inpatient with baseline Cr=1.2 had negative cardiac cath 4 days ago, now Cr=1.8 and blanching rash. Renal Artery Stenosis B. Contrast-Induced Nephropathy C. Abdominal Aortic Aneurysm D. Cholesterol Atheroemboli A. Why do his toes look like this? Renal Atheroembolic Disease 1% of cardiac caths can cause atheromatous debris scraped from the aortic wall will embolize Retinal Cerebral Skin (Livedo Reticularis, Purple toes) Renal (ARF) Gut (Mesenteric ischemia) Unlike in Contrast-Induced Nephropathy, Serum Cr will NOT improve with IVF Diagnosis of exclusion: will NOT show up on MRI or Renal U/S; WILL show up on renal biopsy Treatment is supportive Post-Renal ARF • Urethral obstruction: prostate or urethral stricture • Bladder calculi or neoplasm • Pelvic or retroperitoneal neoplams • Bilateral ureteral obstruction • Retroperitoneal fibrosis “Doc, your patient has not peed in 5 hrs....what do you want to do?” Examine patient: Dry? Septic? Flush foley: sediment can obstruct outflow Check I/Os: Has she been drinking? Give IV BOLUS (250-500cc IVF), see if patient has urine output in next 30-60 min If yes, then patient was dry If no, then patient is either REALLY dry or in renal failure Check UA, Labs Consider Renal U/S if reasonable You are called to the ER to see... A 35yo woman with previously normal renal function now with BUN=60, Cr=3.5. Do you call the Renal fellow to dialyze this pt? What if her K=5.9? What if her K=7.8? Indications for acute dialysis AEIOU Acidosis (metabolic) Electrolytes (hyperkalemia) Ingestion of drugs/Ischemia Overload (fluid) Uremia You admit this patient to telemetry and aggressively hydrate her You recheck labs 6h later and BUN=85, Cr=4.2. Suddenly the patient starts to seize. Now what? Patient is Uremic General Mental status change Uremic encephalopathy Seizures Asterixis GI disturbance Fatigue, weakness Pruritis Anorexia, early satiety, nausea and emesis Uremic Pericarditis Platlet dysfunction and bleeding A patient with chronic lung disease has acute pleuritic pain and O2 saturation of 87%. You want to rule out PE but her Cr is 1.4. Can you get a CT with IV contrast? Send her for Stat CT with IV contrast B. Send her for Stat CT without IV contrast C. Just give her heparin D. Begin IV hydration E. Begin pre-procedure Mannitol F. Get a VQ scan instead A. Contrast-Induced Nephrotoxicity Cr increases by 25% post-procedure Contrast causes renal vasoconstriction leading to renal hypoxia Iodine itself may be nephrotoxic If Cr>1.4, use pre-procedure prophylaxis Pre-Procedure Prophylaxis IVF 0.9NS Mucomyst (N-acetylcysteine) 1-1.5 mg/kg/hour x 12 hours prior to procedure and 612 hours after Free radical scavenger; prevents oxidative tissue damage 600mg po BID x 4 doses (2 before procedure, 2 after) Bicarbonate (JAMA 2004) Alkalinizing urine should reduce renal medullary damage D5W with 3 amps HCO3; bolus 3.5 mL/kg 1 hour preprocedure, then 1mL/kg/hour for 6 hours postprocedure Small study and not reduplicated in larger trial thereafter Chronic Renal Failure Definitions • • • Chronic Renal Failure (CRF) - irreversible kidney dysfunction with azotemia >3 months Creatinine Clearance (CCr) - the rate of filtration of creatinine by the kidney (GFR marker) Glomerular Filtration Rate (GFR) - the total rate of filtration of blood by the kidney Etiology Episodes of ARF (usually acute tubular necrosis) often lead, eventually, to CRF • Over time, combinations of acute renal insults are additive and lead to CRF • The definition of CRF requires that at least 3 months of renal failure have occurred Causes of Acute Renal Failure (ARF) • • • Prerenal azotemia - renal hypoperfusion, usually with acute tubular necrosis Intrinsic Renal Disease, usually glomerular disease Postrenal azotemia - obstruction of some type Common Underlying Causes of CRF Causes of CRF • • There are about 50,000 cases of ESRD per year Diabetes: most common cause ESRD • • • • • • Over 30% cases ESRD are primarily to diabetes CRF associated HTN causes about 23% ESRD cases Glomerulonephritis accounts for ~10% cases Polycystic Kidney Disease - about 5% of cases Rapidly progressive glomerulonephritis (vasculitis) - about 2% of cases Renal (glomerular) deposition diseases Renal Vascular Disease - renal artery stenosis, atherosclerotic vs. fibromuscular Causes of CRF Additional Causes of CRF • • • Medications - especially causing tubulointerstitial diseases (common ARF, rare CRF) Analgesic Nephropathy over many years Pregnancy - high incidence of increased creatinine and HTN during pregnancy in CRF Analgesic Nephropathy Analgesic Nephropathy • • • • • • • Slow progression of disease due to chronic daily ingestion of analgesics Drugs associated with this entity usually contain two antipyretic agents and either caffeine or codeine More common in Europe and Australia than USA Polyuria is most common earliest symptom Macroscopic hematuria and papillary necrosis Chronic interstitial nephritis, renal papillary necrosis, renal calcifications Associated with long-term use of non-steroid antiinflammatory drugs Analgesic Nephropathy Patients at risk include DM, CHF, Hepatic disease, and the elderly Pathophysiology: nonselective NSAIDS inhibit synthesis vasodilatory prostaglandin in the kidney inducing a prerenal state ARF Electrolyte Abnormalities Excretion of sodium is initially increased, probably due to natriuretic factors • • • • • • As glomerular filtration rate (GFR) falls, FeNa rises Maintain urine volume until GFR <10-20mL/min and then edema begins Cannot conserve sodium when GFR <25mL/min, and FeNa rises with falling GFR Tubular potassium secretion is decreased Cannot handle bolus potassium Do not use potassium sparing diuretics Acid Base Balance Normally, produce ~1mEq/kg/day of Hydrogen ions When GFR <40mL/min, there is a decrease in NH4 excretion which adds to metabolic acidosis When GFR <30mL/min, then urinary phosphate buffers decline and acidosis worsens Bone CaCO3 begins to act as the buffer and bone lesions result (renal osteodystrophy) Usually will not have wide anion gap acidosis if patient can still make urine Defect in renal generation of HCO3 as well as retention of nonvolatile acids Bone Metabolism Low GFR leads to increased phosphate, low calcium, and an acidosis Other defects include decreased dihydroxy-vitamin D production Bone acts as a buffer for acidosis, leading to chronic bone loss in renal failure Low vitamin D causes poor calcium absorption and secondary hyperparathyroidism Increased PTH maintains normal serum Calcium and Phosphorus until GFR <30mL/min Chronic hyperparathyroidism and bone buffering of acids leads to severe osteoporosis Other Abnormalities Slight hypermagnesemia with inability to excrete high magnesium loads Uric acid retention occurs with GFR <40mL/min Vitamin D conversion to dihydroxy-Vitamin D is severely decreased Erythropoietin (EPO) levels fall and anemia develops Accumulation of normally excreted substances Complications Immunosuppression • • • • • Patients with CRF are at increased risk for infection Cell mediated immunity is particularly impaired Hemodialysis seems to increase immune compromise Complement system is activated during hemodialysis Patients with CRF should be vaccinated aggressively Anemia Due to reduced erythropoietin production by kidney Occurs when creatinine rises to >2.53mg/dL Anemia management with Procrit and Arensp Phosphorus Hyperphosphatemia • • • • • Decreased excretion by kidney Increased phosphate load from bone metabolism Increased PTH levels leads to renal bone disease Eventually, parathyroid gland hyperplasia occurs Danger of calciphylaxis Treatment PREVENTION Treat the underlying cause Chronic Hemodialysis Medications • • • • • • Anti-hypertensives - Labetolol, CCB, ACE inhibitors Eythropoietin (Epogen®) for anemia in ~80% dialysis pts Vitamin D Analogs - calcitriol given intravenously Calcium carbonate RenaGel, a non-adsorbed phosphate binder DDAVP may be effective for patients with symptomatic platelet problems