A 68-year-old man is admitted to the hospital with acute decompensated heart failure. He is started on an intravenous bumetanide infusion. On hospital day 3, his urine output decreases to 300 mL over the last 24 hours. Physical examination shows jugular venous distention, bibasilar crackles, and bilateral lower extremity pitting edema.
Laboratory studies are obtained:
Serum sodium:
Serum potassium:
Serum chloride:
Serum bicarbonate:
Serum blood urea nitrogen (BUN):
Serum creatinine:
A spot urine sample is analyzed:
Urine sodium:
Urine blood urea nitrogen (BUN):
Urine creatinine:
Based on these findings, what is the patient's fractional excretion of urea nitrogen (expressed as a percentage)?
Answer: 20 %
Answer
20
The correct calculation for the fractional excretion of urea nitrogen is . To determine the etiology of acute kidney injury (AKI) in a patient receiving diuretic therapy, the fractional excretion of urea () should be used rather than the fractional excretion of sodium (). Diuretics impair sodium reabsorption in the tubules, which can falsely elevate the urine sodium concentration and the , masking a prerenal state. Urea reabsorption, primarily occurring in the proximal tubule, is less affected by diuretic use. The formula is . Plugging in the provided values gives . A of less than is indicative of prerenal AKI, which is consistent with this patient's presentation of low forward cardiac output in the setting of acute decompensated heart failure.
Step-by-Step Solution
Key Concept
In patients receiving diuretics who develop acute kidney injury, the fractional excretion of urea () is a more accurate marker for prerenal etiology than the fractional excretion of sodium (). A indicates prerenal AKI.