FENa is one of the oldest and most widely used bedside tests in nephrology: a single paired serum-and-urine sample, plugged into a simple ratio, that helps separate two very different causes of a rising creatinine — reduced blood flow to otherwise-healthy kidneys (prerenal azotemia) versus direct injury to the kidney tissue itself (intrinsic AKI, most often acute tubular necrosis). This guide explains what FENa measures, how to read the result, and where the test breaks down.
What FENa measures
The renal tubules constantly reabsorb the vast majority of the sodium the glomerulus filters — normally more than 99% of it. FENa asks a narrow, specific question: of the sodium filtered, what fraction actually made it into the urine? Creatinine, which is filtered but not meaningfully reabsorbed or secreted under normal conditions, serves as the reference marker for how much fluid was filtered in the first place, so the calculation doesn't require a timed urine collection — a single spot sample of each fluid is enough.
FENa = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100. The formula is the ratio of sodium clearance to creatinine clearance, expressed as a percentage.
How to read the <1% / 1–2% / >2% bands
When blood flow to the kidney is reduced — from dehydration, blood loss, heart failure, or sepsis before frank tubular injury sets in — the tubules respond exactly as they're supposed to: they reabsorb sodium aggressively to help the body conserve volume. FENa in this setting typically runs below 1%.
When the tubules themselves are damaged, as in acute tubular necrosis, that reabsorption machinery is impaired. Filtered sodium that would normally be reclaimed instead escapes into the urine, pushing FENa above 2%. Results between 1% and 2% are genuinely indeterminate — they can occur in early ATN, partial urinary obstruction, contrast-induced nephropathy, or a prerenal state that is starting to transition into tubular injury, and need clinical correlation rather than a clean read.
Why diuretics invalidate FENa (and when to use FEUrea instead)
Loop diuretics (furosemide, bumetanide) and thiazides work by blocking sodium reabsorption directly, which is exactly the variable FENa depends on. A patient who is genuinely volume-depleted but has recently received a diuretic can show a falsely elevated FENa that mimics intrinsic AKI, simply because the drug is forcing sodium out regardless of the underlying cause.
In that setting, the fractional excretion of urea (FEUrea) is the preferred alternative, because urea reabsorption is largely a passive process that diuretics affect much less than they affect sodium transport. See the vs FEUrea tab for the formula and cutoffs.