The diagnosis of acute kidney injury is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests include serum creatinine, blood urea nitrogen (BUN), electrolytes (particularly potassium and bicarbonate), and urine output monitoring. An increase in serum creatinine levels is a hallmark of AKI, though changes in urine output may occur before serum creatinine levels rise.
Urine analysis can provide valuable information, such as the presence of casts (muddy brown casts in ATN), hematuria, pyuria, or proteinuria, which can help differentiate between prerenal and intrinsic causes. Imaging studies such as renal ultrasound or CT scans may be used to evaluate for obstructive causes of AKI, such as kidney stones or tumors.
Newer biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cystatin C, have shown promise in detecting AKI earlier than traditional markers like serum creatinine, although they are not yet widely used in clinical practice.
| Feature | Prerenal | Intrinsic | Postrenal |
|---|---|---|---|
| Primary mechanism | Reduction in renal perfusion | Tubular cell injury from ischemic or toxic insult | Physical obstruction of the urinary tract |
| Consequence for the nephron | Sodium and water are conserved to maintain perfusion; prolonged hypoperfusion causes ischemia and progression to intrinsic AKI | Dead tubular cells slough into the lumen, causing obstruction and back-leak of filtrate and a fall in GFR | Increased hydrostatic pressure reduces filtration |
| Clinical clues | Volume depletion — dry mucous membranes, hypotension, tachycardia | — | Flank pain, hematuria, difficulty voiding |
| Supporting studies | Urinalysis helps separate prerenal from intrinsic causes | Muddy brown casts on urinalysis in acute tubular necrosis | Renal ultrasound or CT to identify stones or tumors |
