Acute kidney injury is sudden loss of GFR function caused by prerenal hypoperfusion, intrinsic kidney damage, or postrenal obstruction. Acute tubular necrosis is the most common pathology, characterized by epithelial cell injury and loss of barrier function.
Use BUN/Creatinine ratio to distinguish prerenal from intrinsic AKI. Examine urinalysis (muddy casts in ATN, proteinuria in glomerulonephritis). Understand RIFLE and KDIGO criteria for severity staging.
Mild serum creatinine elevation does not exclude severe AKI—the rate of rise matters. Oliguria is not required for AKI diagnosis; non-oliguric AKI has better prognosis.
You already know that the kidney maintains fluid balance and excretes waste by filtering blood through glomeruli, reabsorbing what the body needs in the tubules, and excreting the rest as urine. The key measure of this work is glomerular filtration rate (GFR) — roughly 120 mL/min in a healthy adult. Acute kidney injury (AKI) is a sudden, sustained fall in GFR, defined operationally by a rise in serum creatinine or a fall in urine output. Because creatinine is normally excreted entirely by the kidney, any reduction in filtration causes it to accumulate in the blood — making it a convenient biomarker of kidney function.
Clinicians organize the causes of AKI into three anatomical categories based on where the problem originates. Prerenal AKI is the most common: reduced blood flow to the kidney — from dehydration, hemorrhage, heart failure, or sepsis — drops the perfusion pressure that drives filtration. The kidney itself is structurally normal; it simply isn't getting enough blood. Intrinsic renal AKI involves damage to kidney tissue itself. The most common cause is acute tubular necrosis (ATN), in which prolonged ischemia or nephrotoxins (contrast agents, aminoglycoside antibiotics, myoglobin from rhabdomyolysis) injure the tubular epithelial cells, causing them to slough into the tubule lumen and obstruct flow. Postrenal AKI results from obstruction downstream of the kidney — a kidney stone, enlarged prostate, or tumor blocking urinary drainage; back-pressure builds up and impairs filtration.
Distinguishing these categories determines treatment. The BUN-to-creatinine ratio is a first-pass tool: in prerenal AKI, the kidney is intact and over-reabsorbs urea (BUN) in its attempt to conserve volume, so BUN rises disproportionately to creatinine, giving a ratio >20:1. In ATN, tubular reabsorption is impaired, so BUN does not accumulate as disproportionately. Urinalysis adds specificity: ATN produces pathognomonic "muddy brown" granular casts from sloughed tubular cells; glomerulonephritis produces red blood cell casts; prerenal AKI typically shows bland urine with hyaline casts.
AKI severity is staged using KDIGO criteria: Stage 1 is a creatinine rise of 0.3 mg/dL within 48 hours or 1.5–1.9× baseline; Stage 2 is 2–2.9× baseline; Stage 3 is 3× baseline, creatinine ≥4 mg/dL, or requirement for renal replacement therapy. The critical clinical insight — captured in the Common Misconceptions — is that even modest creatinine elevations can mask severe injury: because creatinine must accumulate in a large volume of distribution, the absolute creatinine level lags behind the rate of GFR decline. A rapidly rising creatinine from 1.0 to 2.0 mg/dL may represent more acute injury than a stable creatinine of 3.0 mg/dL in a patient with chronic kidney disease.