Snapshot A 44-year-old woman with no significant past medical history presents to the emergency room with toxic ingestion of ethylene glycol. She answers appropriately but requires frequent redirection. Physical exam reveals bilateral flank pain. Her serum creatinine, previously normal, is now increased at 3 mg/dL. Urinalysis with sediment analysis reveals granular casts and significant hematuria. Fomepizole is given. Introduction Clinical definition intrinsic acute kidney injury (AKI) to the kidneys from ischemia and/or toxins Epidemiology incidence US incidence 38% of hospitalized patients with AKI 76% of ICU patients with AKI most common cause of AKI in hospitalized patients risk factors pre-existing kidney disease exposure to nephrotoxin Etiology ischemia hypovolemia sepsis nephrotoxic injury drugs aminoglycosides cisplatin contrast for imaging heavy metals calcium oxalate crystals from ethylene glycol urate crystals from tumor lysis syndrome myoglobinuria (from crush injury) hemoglobinuria Pathogenesis decreased renal blood flow results in ischemia this results in death of renal tubular cells in particular proximal convoluted tubule and thick ascending limb are affected nephrotoxicity leads to damage in renal tubules in particular proximal convoluted tubule is affected Prognosis 3 stages of disease inciting event oliguric (maintenance) phase 1-3 week duration risk of electrolyte abnormalities hyperkalemia metabolic acidosis uremia polyuric (recovery) phase BUN and creatinine return back to normal re-epithelialization of tubules risk of hypokalemia prognostic variable negative pre-existing renal disease requiring dialysis survival with treatment over half of patients fully recover 5-11% require long-term dialysis 50% mortality in those needing dialysis Classification of Acute Renal FailuresUrinary IndicesPre-RenalIntrinsic RenalPost-RenalUrine osmolality (mOsm/kg)> 500< 350< 350Urine Na (mEq/L)< 20> 40> 40Serum BUN:creatinine> 20< 15< 15FENa (%)(fractional excretion of Na)< 1%> 2%> 2%FEUrea (%) (fractional excretion of urea)< 35%50-65 %- Presentation Symptoms primary symptoms signs of acute renal failure vomit diarrhea blood loss shock altered mental status oliguria or polyuria Physical exam signs of volume overload edema jugular venous distention decreased breath sounds in pulmonary edema Imaging Ultrasound indications if an obstruction needs to be ruled out (post-renal cause of AKI) best initial test findings can see hydronephrosis or stones Studies Labs serum potassium hyperkalemia during oliguric phase hypokalemia during polyuric phase anion gap metabolic acidosis ↑ BUN ↑ creatinine BUN:creatinine ratio < 15 Urinalysis with microscopy and sediment analysis granular casts “muddy brown” from sloughing of tubular cells Diagnostic criteria diagnosis of AKI ↑ serum creatinine of ≥ 0.3 mg/dL within 48 hours ↑ serum creatinine of 1.5 fold from baseline signs of acute tubular necrosis urine osmolality < 350-500 mOsm/kg muddy brown casts on urine sediment analysis fractional excretion of sodium > 2% decreased BUN:creatinine ratio Differential Prerenal azotemia BUN:creatinine ratio > 20 Post-renal azotemia source of obstruction found on imaging e.g., stones or congenital abnormality Treatment Conservative supportive care remove nephrotoxic agent intravenous hydration close electrolyte and fluid level monitoring anitbiotics if infection is suspected indications for all with suspected acute tubular necrosis Medical renal replacement therapy (dialysis) indications signs of fluid overload toxic electrolyte levels acid-base imbalance uremia Complications Electrolyte abnormalities hypokalemia hyperkalemia Volume overload Uremia