Acute kidney injury in a patient with severe dehydration is most likely due to which type of azotemia?

• A. Prerenal azotemia
• B. Intrinsic renal azotemia
• C. Postrenal obstruction
• D. Hepatorenal syndrome

Answer: (A)

Dehydration lowers effective circulating volume and renal perfusion, so the kidneys conserve water and Na to preserve blood pressure and GFR. This hemodynamic response increases reabsorption of urea in the nephron, causing nitrogenous waste to accumulate with a disproportionately high BUN relative to creatinine. The result is prerenal azotemia.

Clinical clues fit this pattern: urine is typically concentrated with low urine sodium and a BUN:creatinine ratio greater than 20:1, and the fractional excretion of sodium is low (<1%). If perfusion remains severely reduced for a longer period, tubular injury can develop, but the immediate mechanism in dehydration is prerenal due to decreased renal perfusion, not intrinsic tubular damage or obstruction.

Intrinsic renal azotemia would show a higher FeNa (often >2%), urine findings like granular casts, and a less elevated BUN:Cr ratio. Postrenal obstruction and hepatorenal syndrome have distinct contexts and lab/imaging features that don’t align with simple dehydration.