This post is somewhat basic but it’s always good to review, right?The FENa is one of the most commonly used tools by both nephrologists and non-nephrologists to assess the etiology of oliguric renal failure in a patient. Classically, a FENa less than 1% is consistent with pre-renal etiologies (and means that more than 99% of the Na filtered is being reabsorbed) while a FENa greater than 1% is consistent with acute tubular necrosis or other types of intrinsic renal failure. There are however some specific instances in which the FENa fails. FENa “false positives” (e.g., the FENa is less than 1% but the patient actually has intrinstic renal failure) in the folllowing conditions. Contrast nephropathy is notorious for causing a FENa less than 1% despite its not being classified as a true pre-renal etiology of renal failure. Patients with CHF or cirrhosis/hepatorenal syndrome who develop ATN with clear evidence of granular casts may still retain a FENa less than 1%. Acute glomerulonephritis and rhabdomyolysis may also result in FENa’s less than 1%. Conversely, FENa “false negatives” (e.g., the FENa is greater than 1% but the patient is actually pre-renal) frequently occur due to one very common cause: diuretics. In the face of active diuretic use, a FENa greater than 1% is therefore uninterpretable, and one popular alternative is to assess the fractional excretion of urea (FE-urea). Since urea is reabsorbed less avidly than sodium, the cutoffs for what constitutes pre-renal and renal etiologies are different: a FE-urea greater than 35% is consistent with intrinstic renal failure while a FE-urea less than 35% is consistent with pre-renal failure. On a previous post I noted the problems inherent in using the FENa is patients with significant chronic kidney disease.