ACUTE RENAL FAILURE

.Background ‡ Reversible illness ‡ Common in Hospitalized patients ‡ Associated with high Morbidity and Mortality ‡ Often Multifactorial ‡ Identifiable risk factors.

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Acute Renal Failure ‡ Sudden decrease kidney function (hoursdays) ‡ Often multifactorial ‡ Pre-renal and intrinsic renal causes : 70% ‡ oliguric UOP < 400-500 ml (35%) ‡ Non-oliguric (up to 65%) ‡ Associated with high mortality and morbidity. if not tted properly .

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Catabolic state. hypovolemia ± BUN/Cr ratio helpful in classifying cause of ARF ‡ ratio> 20:1 suggests prerenal cause ‡ ratio 10-15:1 suggests intrinsic renal cause . GIB. More reliable marker of GFR ‡ small change reflects large change in GFR ± BUN/urea.Acute Renal Failure Diagnosis ‡ Laboratory Evaluation: ± Scr. generally follows Scr increase ‡ Elevation may be independent of GFR ( normal kidney function but high urea/bun) ± Steroids.

AGN ‡ Muddy brown casts in ATN ‡ WBC casts in AIN . pre and post renal causes ± Renal ± Differentiates ATN vs. vs. AIN.Acute Renal Failure Diagnosis (cont¶d) ‡ Urinalysis ± MAY BE NORMAL in.

‡ high BUN/creat ratio. Diuretic use...Prerenal ARF ‡ Nearly as common as ATN (think of as early part of the disease spectrum) ‡ Diagnose by history and physical exam ± N/V.. ‡ normal urinary sediment ‡ Treat: correction of predisposing factors . Diarrhea.

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sepsis. Heme proteins ‡ COMBINATION OF BOTH. carries better prognosis (1) Ischemic ATN: ‡ Hypotension. prolonged pre-renal state ± (2) Nephrotoxic ATN: ‡ Contrast/ DYE.Acute Renal Failure Etiologies ‡ Acute Tubular Necrosis ± ± ± ± Most common intrinsic ARF Often multifactorial LOW URINE OUTPUT. Antibiotics. MANY TIMES .

2 ‡ Diagnose by history. if initial insult treated aggressively . ± (1)Maintenance of euvolemia /normal body volume (with judicious use of diuretics. ‡ Treatment. as necessary) ± (2) Treat. ‡ Urine sediment with coarse granular casts. ‡ (A) supportive care.Acute Tubular Necrosis (ATN) -. hypotension ± (3) Avoid. if no recovery ‡ OUTCOME: 80% will recover. IVF. nephrotoxic drugs (including NSAIDs and ACE-I) when possible ± (B) Dialysis.

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peaks in 3-5 days ‡ Non-oliguric ‡ treatment/Prevention: 1/2 NS 1 cc/kg/hr 12 hours pre/post ‡ Mucomyst 600 BID pre/post (4 doses) ‡ Risk Factors: CRF./DM .Contrast nephropathy ‡ 12-24 hours post exposure. Hypovolemia.

Rhabdomyolytic ARF ‡ CAUSE : after trauma (³crush injuries´). ‡ pigmented granular casts ‡ Treatment. seizures. ‡ urine dipstick (+) for blood. HYDRATION & Alkalinization of urine . burns ‡ Diagnose: ‡ o serum CPK (usu. without RBCs on microscopy.000). > 10. .

NSAIDS ± Develops 3-7 days after exposure ± Fever. WBC casts.5 mg/dl) . + Hansel stain ± Treatment: Often resolves spontaneously ± Steroids may be beneficial ( if Scr>2.Acute Interstitial Nephritis ± Usually drug induced ‡ methicillin. and eosinophilia common ± Urine: reveals WBC. Rash . rifampin.

Indanivir. intrapelvic pathology ± Crystalluria (DRUGS) ‡ Acyclovir. Uric Acid .Acute Renal Failure Etiologies ‡ Post-Renal ± Bladder outlet obstruction ‡ BPH.

Prevention What works? ‡ Maintenance of euvolemia ‡ Avoidance of nephrotoxins when possible ± NSAIDs. IV contrast ‡ BP control--avoidance of excessive hypoor hypertension . Amphotericin. aminoglycoside.

.Prevention What doesn¶t work? ‡ Empiric use of: ± Diuretics (i. Mannitol) ± Dopamine (or Dopamine agonists such as Fenoldopam) ± Calcium-channel blockers .e. ? Furosemide.

Acute Renal Failure Treatment ‡ ‡ ‡ ‡ ‡ Water and sodium restriction Protein restriction Potassium and phosphate restriction Adjust medication dosages Avoidance of further insults ± BP support ± Nephrotoxins .

5 meq/L needs evaluation/intervention .Hyperkalemia ‡ Dangerous to heart ‡ Highly Arrhythmogenic ± ECG changes ‡ Peaked T waves ---> Widened QRS--> Sinus wave ± K> 5.

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Dialysis Indications ‡ Refractory hyperkalemia ‡ Metabolic acidosis ‡ Volume overload ‡ Mental status changes .

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