3 learning resources available for this topic
Acute kidney injury (AKI) is a sudden decline in kidney function, defined by a rise in serum creatinine or reduction in urine output over hours to days. It complicates up to 20% of hospital admissions and is independently associated with increased mortality, chronic kidney disease progression, and length of stay.
AKI is categorized by mechanism: prerenal (reduced renal perfusion from volume depletion, heart failure, or hepatorenal syndrome), intrinsic (tubular injury from ischemia or nephrotoxins, glomerulonephritis, interstitial nephritis), or postrenal (urinary tract obstruction). Ischemic and nephrotoxic acute tubular necrosis (ATN) accounts for the majority of intrinsic AKI in hospitalized patients.
Clinical reasoning relies on the fractional excretion of sodium (FENa <1% suggests prerenal, >2% suggests ATN), urine sediment (granular muddy brown casts suggest ATN; RBC casts suggest glomerulonephritis), and response to fluids. Timing and context are critical — contrast administration, aminoglycosides, and NSAIDs suggest nephrotoxic ATN. Bladder ultrasound rules out obstruction. AKI staging by KDIGO criteria (creatinine and UOP) guides intensity of monitoring and renal replacement therapy decisions.
Common clinical reasoning questions about this topic
KDIGO defines AKI as increase in serum creatinine ≥0.3 mg/dL within 48 hours, or ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 hours.
FENa <1% suggests prerenal (kidneys avidly retaining sodium), while FENa >2% suggests ATN. However, FENa can be falsely low in contrast nephropathy and myoglobinuria. Urine sediment showing granular muddy brown casts strongly suggests ATN.
Common nephrotoxic medications include NSAIDs (reduce renal prostaglandins), ACE inhibitors/ARBs (reduce GFR in low-flow states), aminoglycosides (proximal tubular toxicity), vancomycin, contrast agents, and calcineurin inhibitors.