fractional excretion of sodium

FENa = [(Urine Na x Plasma Cr) / (Plasma Na x Urine Cr)] x 100. It reflects the percentage of filtered sodium that is excreted in the urine, serving as a marker of renal tubular function relative to glomerular filtration.

Pathophysiology: In prerenal azotemia (e.g., due to volume depletion, heart failure, cirrhosis), renal perfusion is reduced but tubular function remains intact. This triggers increased aldosterone and ADH activity, leading to avid sodium and water reabsorption, resulting in low urine sodium and FENa <1%. In contrast, intrinsic renal injury such as ATN damages the tubular epithelium, impairing sodium reabsorption despite ongoing filtration, leading to urinary sodium wasting and FENa >2%.

Clinical use: FENa is most useful in oliguric acute kidney injury when trying to distinguish prerenal azotemia from ATN. It is less reliable in patients on diuretics (which cause natriuresis independent of tubular injury) or in chronic kidney disease, contrast-induced nephropathy, or hepatorenal syndrome (may show low FENa despite intrinsic pathology). In diuretic-treated patients, fractional excretion of urea (FEUrea) is preferred, with FEUrea <35% suggesting prerenal etiology.

Other supportive findings: BUN/Cr ratio >20:1, urine specific gravity >1.020, and bland urine sediment suggest prerenal azotemia; muddy brown granular casts and epithelial cell casts suggest ATN.

High-yield board points: FENa <1% = prerenal; FENa >2% = ATN/intrinsic; FENa 1-2% = indeterminate zone. Remember exceptions: diuretics, contrast nephropathy, myoglobinuria, and early obstruction can confound interpretation.