Step 1: Understand pre-renal azotemia. It is a fall in renal perfusion (volume loss, hypotension, heart failure) with intact tubular function. The kidney responds by avidly conserving sodium and water to defend blood volume.
Step 2: Predict the urine indices. Because the tubules reabsorb sodium hard, the urine has very little sodium. Therefore fractional excretion of sodium falls below 1 percent (option A is true) and urinary sodium concentration is low, typically less than 20 meq/l.
Step 3: Predict urine concentration. With intact tubules and high ADH drive, the kidney concentrates urine strongly, so urinary osmolality rises above 500 mosm/kg (option B is true).
Step 4: Apply reversibility. Pre-renal azotemia, by definition, corrects once perfusion is restored with fluids, before tubular injury sets in (option D is true).
Step 5: Find the exception. A urinary sodium concentration above 40 meq/l indicates sodium wasting, which is a feature of intrinsic acute tubular necrosis, not pre-renal disease. So option C is the odd one out.
The answer is option C.