Internal medicine/Nephrology Wake Forest University School of Medicine Background • Common in Hospitalized patients • Associated with high Morbidity and Mortality • Often Multifactorial • Identifiable risk factors. Acute Renal Failure • Sudden decrease in function (hours-days) • Often multifactorial • Pre-renal and intrinsic renal causes 70% • oliguric UOP < 400 ml • Non-oliguric (up to 65%) • Associated with high mortality and morbidity Acute Renal Failure Diagnosis • Laboratory Evaluation: – Scr, More reliable marker of GFR • Falsely elevated with Septra, Cimetidine • small change reflects large change in GFR – BUN, generally follows Scr increase • Elevation may be independent of GFR – Steroids, GIB, Catabolic state, hypovolemia – BUN/Cr helpful in classifying cause of ARF • ratio> 20:1 suggests prerenal cause • ratio 10-15:1 suggests intrinsic renal cause Acute Renal Failure Diagnosis (cont’d) • Urinalysis – Unremarkable in pre and post renal causes – Differentiates ATN vs. AIN. vs. AGN • Muddy brown casts in ATN • WBC casts in AIN – Hansel stain for Eosinophils Acute Renal Failure Diagnosis (cont’d) • Urinary Indices; – FE Na = (U/P) Na X (P/U)CrX 100 • FENa < 1% C/W Pre-renal state – May be low in selected intrinsic cause » Contrast nephropathy » Acute GN » Myoglobin induced ATN • FENa> 1% C/W intrinsic cause of ARF Prerenal Azotemia • Nearly as common as ATN (think of as early part of the disease spectrum) • Diagnose by history and physical exam – N/V, Diarrhea, Diuretic use,... • low FENa (<1%) • high BUN/creat ratio, normal urinary sediment • Treat by correction of predisposing factors Acute Renal Failure Etiologies • Acute Tubular Necrosis – Most common cause of intrinsic cause of ARF – Often multifactorial – Non-oliguria carries better prognosis – Ischemic ATN: • Hypotension, sepsis, prolonged pre-renal state – Nephrotoxic ATN: • Contrast, Antibiotics, Heme proteins Acute Tubular Necrosis (ATN) -- 2 • Diagnose by history, FENa (>2%) • sediment with coarse granular casts, RTE cells • Treatment is supportive care. – Maintenance of euvolemia (with judicious use of diuretics, IVF, as necessary) – Avoidance of hypotension – Avoidance of nephrotoxic medications (including NSAIDs and ACE-I) when possible – Dialysis, if necessary • 80% will recover, if initial insult can be reversed. Contrast nephropathy • 12-24 hours post exposure, peaks in 3-5 days • Non-oliguric, FE Na <1% !! • RX/Prevention: 1/2 NS 1 cc/kg/hr 12 hours pre/post • Mucomyst 600 BID pre/post (4 doses) • Risk Factors: CRF, Hypovolemia. Rhabdomyolytic ARF • Diagnose with serum CPK (usu. > 10,000), urine dipstick (+) for blood, without RBCs on microscopy, pigmented granular casts • Common after trauma (“crush injuries”), seizures, burns, limb ischemia occasionally after IABP or cardiopulmonary bypass • Treatment is largely supportive care. • Alkalinization of urine . Acute Glomerulonephritis • Rare in the hospitalized patient • Most common types: acute post-infectious GN, “crescentic” RPGN • Diagnose by history, hematuria, RBC casts, proteinuria (usually non-nephrotic range), low serum complement in post-infectious GN), RPGN often associated with anti-GBM or ANCA • Usually will need to perform renal biopsy Acute Glomerulonephritis (2) • If diagnosis is post-infectious, disease is usually self-limited, and supportive care is usually all that is necessary. • For RPGN, may need immunosuppressive therapy with steroids ± Cytoxan, plasmapheresis (if assoc. with anti-GBM) Atheroembolic ARF • Associated with emboli of fragments of atherosclerotic plaque from aorta and other large arteries • Diagnose by history, physical findings (evidence of other embolic phenomena--CVA, ischemic digits, “blue toe” syndrome, etc), low serum C3 and C4, peripheral eosinophilia, eosinophiluria, rarely WBC casts • Commonly occur after intravascular procedures or cannulation (cardiac cath, CABG, AAA repair, etc.) Acute Interstitial Nephritis – Usually drug induced • methicillin, rifampin, NSAIDS – Develops 3-7 days after exposure – Fever, Rash , and eosinophilia common – U/A reveals WBC, WBC casts, + Hansel stain – Often resolves spontaneously – Steroids may be beneficial ( if Scr>2.5 mg/dl) Acute Renal Failure Etiologies • Post-Renal – Bladder outlet obstruction • BPH, intrapelvic pathology – Crystalluria • Acyclovir, Indanivir, Uric Acid – Papillary tip necrosis • DM with pyelonephritis • Analgesic abuse • Sickle cell disease Prevention What works? • Maintenance of euvolemia • Avoidance of nephrotoxins when possible – NSAIDs, aminoglycoside, Amphotericin, IV contrast • BP control--avoidance of excessive hypo- or hypertension Prevention What doesn’t work? • Empiric use of: – Diuretics (i.e., Furosemide, Mannitol) – Dopamine (or Dopamine agonists such as Fenoldopam) – Calcium-channel blockers Acute Renal Failure Treatment • Water and sodium restriction • Protein restriction • Potassium and phosphate restriction • Adjust medication dosages • Avoidance of further insults – BP support – Nephrotoxins Hyperkalemia • Highly Arrhythmogenic – Usually with progressive EKG changes • Peaked T waves ---> Widened QRS--> Sinus wave – K> 5.5 meq/L needs evaluation/intervention – Usually in setting of Decrease GFR but: • medication also a common cause – ACEI – NSAIDS – Septra, Heparin Dialysis Indications • Refractory hyperkalemia