Acute Kidney Injury (AKI) is defined by a rapid decline in glomerular filtration rate (GFR) over hours to days, resulting in retention of nitrogenous waste products (azotemia) and dysregulation of fluid, electrolyte, and acid-base balance. The KDIGO criteria define AKI as: increase in serum creatinine by >=27 µmol/L within 48 hours, OR increase to >=1.5x baseline within 7 days, OR urine output <0.5 mL/kg/hr for 6 hours. AKI is classified by etiology: (1) Prerenal AKI (55-60% of cases): decreased renal perfusion from hypovolemia, heart failure, sepsis, or renal artery stenosis. The kidney is structurally intact but underperfused. BUN/creatinine ratio is >20:1 because the kidney reabsorbs urea in response to decreased perfusion. (2) Intrarenal/intrinsic AKI (35-40%): direct damage to the nephron structures. Acute tubular necrosis (ATN) is the most common cause, resulting from ischemia (prolonged prerenal state) or nephrotoxins (aminoglycosides, contrast dye, myoglobin from rhabdomyolysis). Muddy brown granular casts in urinalysis are pathognomonic for ATN. (3) Postrenal AKI (5-10%): mechanical obstruction to urine outflow - BPH, kidney stones, tumors, or blood clots. Bilateral obstruction (or unilateral in a single kidney) is...