Health & Medical

FENa Calculator

Calculate FENa instantly to differentiate pre-renal azotemia from acute tubular necrosis in AKI.

Urine Values
mEq/L
mg/dL
Serum / Plasma Values
mEq/L
mg/dL
FENa
%
Likely Cause

The FENa calculator (Fractional Excretion of Sodium) estimates the percentage of filtered sodium excreted in urine, helping to distinguish prerenal azotemia from intrinsic acute tubular necrosis in acute kidney injury.

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This team builds, tests, and maintains free online calculators designed to make everyday calculations faster, simpler, and reliable for users around the world.

A creatinine that’s suddenly climbing raises one immediate question: is this kidney hypoperfused, or is the kidney itself injured? A FENa calculator answers that by comparing how much sodium the kidney is excreting against how much it’s filtering — a ratio that behaves very differently depending on which of those two problems is actually happening.

From four lab values to one percentage

FENa (%) = (Urine Na × Plasma Cr) ÷ (Plasma Na × Urine Cr) × 100. Creatinine in both the numerator and denominator just needs to use matching units — mg/dL and mg/dL, or µmol/L and µmol/L — since the units cancel out in the ratio and only the relative values matter.

Worked example: calculating FENa

Prerenal pattern: Urine Na 15 mEq/L, Plasma Na 138 mEq/L, Urine Cr 60 mg/dL, Plasma Cr 2.4 mg/dL. FENa = (15 × 2.4) ÷ (138 × 60) × 100 = 36 ÷ 8,280 × 100 = 0.43% — consistent with a prerenal cause and avid tubular sodium reabsorption.

ATN pattern: Urine Na 60 mEq/L, Plasma Na 135 mEq/L, Urine Cr 40 mg/dL, Plasma Cr 3.0 mg/dL. FENa = (60 × 3.0) ÷ (135 × 40) × 100 = 180 ÷ 5,400 × 100 = 3.33% — consistent with tubular injury, since damaged tubules have lost the ability to reabsorb filtered sodium.

Interpreting the result: prerenal azotemia vs. ATN

FENa Typical interpretation
< 1% Prerenal azotemia — hypovolemia, CHF, cirrhosis, sepsis-related hypoperfusion, renal artery stenosis
1–2% Indeterminate zone; overlaps both categories, needs clinical correlation
> 2% Intrinsic renal injury — most commonly acute tubular necrosis (ATN)

No single FENa value rules a diagnosis in or out on its own. It’s one data point that gets weighed alongside history, exam findings, urine sediment, and the trajectory of the creatinine itself.

Why a value under 1% actually means something

The cutoff isn’t arbitrary. At a normal glomerular filtration rate of about 180 L/day and a serum sodium of 140 mEq/L, the kidney filters roughly 26,100 mEq of sodium per day. A FENa of 1% in that setting means excreting about 261 mEq/day — more sodium than a typical 80–250 mEq/day dietary intake.

A FENa meaningfully below 1% means the tubules are reabsorbing sodium far more aggressively than baseline intake would require — exactly what you’d expect from a kidney responding appropriately to reduced perfusion, not one that’s structurally damaged.

When FENa stops being reliable

FENa is built for one specific situation: oliguric acute kidney injury (urine output under 0.5 mL/kg/hr), without diuretics, CKD, obstruction, or active glomerular disease clouding the picture. Outside that window, the number gets harder to trust.

Several conditions produce a low FENa despite genuine intrinsic kidney injury — contrast-induced nephropathy, rhabdomyolysis, early acute interstitial nephritis, acute glomerulonephritis, and cardiorenal or hepatorenal syndrome can all mimic the prerenal pattern even though the kidney itself is the problem. Chronic tubular injury and diuretic use work the other way, elevating FENa despite a genuinely prerenal, volume-depleted state.

FEUrea: the workaround for patients on diuretics

Loop and thiazide diuretics block sodium reabsorption directly, which pushes FENa up regardless of volume status and makes the test unusable. Fractional excretion of urea isn’t affected the same way, since urea reabsorption happens largely in the proximal tubule, upstream of where most diuretics act.

FEUrea below 35% suggests a prerenal process; above 50% suggests intrinsic injury. It’s the standard substitute whenever a patient has already received diuretics before the urine studies were collected — which, in practice, is often the case by the time AKI gets worked up in the hospital.

  • FENa does not have a "normal" range in healthy individuals — it is a diagnostic tool used specifically in the context of acute kidney injury. A value below 1% suggests pre-renal azotemia, meaning the kidneys are intact but underperfused. A value above 2% points toward intrinsic renal damage such as acute tubular necrosis.

  • No — diuretics artificially raise urine sodium excretion, which falsely elevates FENa regardless of true volume status. In patients who have received loop diuretics or thiazides within the past 24–48 hours, FEUrea is the preferred alternative. A FEUrea below 35% suggests pre-renal physiology even in the presence of diuretics.

  • FENa requires urine sodium (mEq/L), urine creatinine (mg/dL), serum sodium (mEq/L), and serum creatinine (mg/dL). All four values should be collected from simultaneous or near-simultaneous samples for the result to be clinically valid.

  • Several conditions cause ATN-pattern injury while still producing a FENa below 1% — including early contrast-induced nephropathy, myoglobinuric renal failure, and hepatorenal syndrome. In these cases, tubular sodium reabsorption remains partially or fully intact despite significant renal injury. This is why FENa must always be interpreted alongside clinical history and urine microscopy, not in isolation.

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