The answer is C. A urine osmolality of 620 mOsm/kg
A urine osmolality of 620 mOsm/kg supports a prerenal cause, because it proves the tubules are still working. That single idea unlocks the entire prerenal-versus-ATN table: in prerenal azotemia the kidney is structurally intact and appropriately hypoperfused, so it does exactly what a healthy kidney should do when volume is low — it avidly reabsorbs sodium and concentrates urine. In acute tubular necrosis the tubular cells are injured and can no longer reabsorb sodium or generate a concentration gradient, so sodium is wasted and the urine drifts toward isosthenuria, roughly the osmolality of plasma at about 300 mOsm/kg.
Memorize the table as one physiologic story rather than ten numbers:
Prerenal — BUN:creatinine ratio >20:1, urine sodium <20 mEq/L, FENa <1%, urine osmolality >500 mOsm/kg, specific gravity >1.020, and a bland sediment with at most hyaline casts.
ATN — BUN:creatinine ratio 10 to 15:1, urine sodium >40 mEq/L, FENa >2%, urine osmolality <350 mOsm/kg, specific gravity near 1.010, and muddy brown granular casts with renal tubular epithelial cells.
The disproportionate BUN rise in prerenal disease is not incidental: reabsorbing sodium and water in the proximal tubule drags urea back with it, which is why urea climbs faster than creatinine and pushes the ratio above 20:1. Two important caveats on FENa: it is invalid in a patient already given a diuretic, in whom you should use the fractional excretion of urea (FEUrea <35% suggests prerenal) instead; and a FENa under 1% can also occur in contrast nephropathy, hepatorenal syndrome, and acute glomerulonephritis, so it is supportive rather than definitive.
This patient’s medications matter clinically even though they are not the answer. NSAIDs constrict the afferent arteriole and ACE inhibitors dilate the efferent arteriole; together they strip the kidney of both autoregulatory defenses and convert ordinary volume depletion into acute kidney injury. Hold both, restore volume with isotonic crystalloid, and recheck — prerenal azotemia reverses promptly with perfusion, and failure to improve after adequate resuscitation is what tells you ATN has already set in.
Sorting the distractors: a urine sodium of 55 mEq/L shows sodium wasting and points to ATN, since a hypoperfused intact kidney should be holding sodium below 20; a FENa of 3.5% likewise indicates that the tubules have lost their reabsorptive capacity and is well into the ATN range above 2%; muddy brown granular casts are the hallmark sediment finding of ATN, formed from sloughed tubular epithelial cells, whereas prerenal sediment is bland; and a urine specific gravity of 1.008 is dilute, essentially isosthenuric, and again indicates a kidney that has lost its ability to concentrate — the opposite of prerenal physiology.
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