Snapshot A 52-year-old man with a past medical history of diabetes mellitus presents with fever and acute onset left lower quadrant abdominal pain. CT scan with contrast shows acute diverticulitis. He is started on broad-spectrum antibiotics. The next day, daily labs reveal a rise in creatinine from 0.7 mg/dL to 2.0 mg/dL. Urinalysis is obtained and a significant amount of muddy brown casts is found. He is immediately started on intravenous normal saline. Introduction Clinical definition intrinsic acute kidney injury (AKI) to the kidneys from ischemia and/or toxins Epidemiology incidence US incidence most common cause of AKI in hospitalized patients risk factors pre-existing kidney disease Etiology ischemia hypovolemia sepsis nephrotoxic injury drugs aminoglycosides contrast for imaging heavy metals crystals calcium oxalate crystals from ethylene glycol urate crystals from tumor lysis syndrome myoglobinuria hemoglobinuria Pathogenesis decreased renal blood flow results in ischemia this results in death of renal tubular cells in particular the 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 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 Failures Urinary Indices Pre-Renal Intrinsic Renal Post-Renal Urine osmolality (mOsm/kg) > 500 < 350 < 350 Urine Na (mEq/L) < 20 > 40 > 40 Serum BUN:creatinine > 20 < 15 < 15 FENa (%)(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 Histology rarely obtained unless concerned about a concurrent glomerular process will show necrosis of tubular lining cells 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 indications for all with suspected acute tubular necrosis Medical renal replacement therapy (dialysis) indications signs of fluid overload toxic electrolyte levels Complications Electrolyte abnormalities hypokalemia hyperkalemia Volume overload