Medical AIFractional excretion of sodium (FENa)
FENa is the percentage of filtered sodium that ends up in the urine. In oliguric acute kidney injury a value below 1% points to prerenal azotemia (kidneys avidly reabsorbing sodium in response to hypoperfusion), while a value above 2% suggests intrinsic tubular injury such as acute tubular necrosis. It was derived in selected oliguric patients and is unreliable in several common situations, most notably diuretic use.
How to measure each input
- Paired samples
- Send a spot urine sodium and creatinine together with a serum sodium and creatinine drawn at about the same time, ideally before fluids or diuretics shift the values.
- Consistent creatinine units
- Use the same unit for urine and plasma creatinine (mg/dL in this tool). The creatinine unit cancels in the ratio, so only the sodium values need to be in mmol/L.
- Oliguric setting
- FENa was validated in the oliguric phase of acute renal failure. It is most informative when urine output is low; in non-oliguric injury its discrimination is weaker.
Interpretation
| Band | Meaning |
|---|---|
| FENa < 1%, suggests prerenal azotemia | A FENa below 1% indicates avid tubular sodium reabsorption, typical of prerenal azotemia from hypovolaemia, hypotension, heart failure, or cirrhosis. Note that some intrinsic causes (contrast nephropathy, early glomerulonephritis, rhabdomyolysis) can also give a low FENa. |
| FENa 1 to 2%, indeterminate | An intermediate FENa does not reliably distinguish prerenal from intrinsic injury. Interpret alongside the clinical picture, urine microscopy, response to a fluid challenge, and, if diuretics are in play, the fractional excretion of urea. |
| FENa > 2%, suggests intrinsic renal injury / ATN | A FENa above 2% suggests impaired tubular sodium reabsorption, classically acute tubular necrosis. Confirm with urine sediment (muddy-brown granular casts) and the clinical course rather than on the number alone. |
Pitfalls, exclusions and caveats
- Invalid in patients on diuretics: loop and thiazide diuretics raise urine sodium and push FENa above 1% even when the patient is prerenal. In that setting use the fractional excretion of urea (FEUrea), where a value below 35% supports prerenal azotemia (Carvounis et al. 2002).
- A low FENa is not specific for prerenal disease: contrast-induced nephropathy, early or acute glomerulonephritis, rhabdomyolysis, and hepatorenal syndrome can all produce FENa below 1% despite intrinsic kidney involvement.
- Unreliable in chronic kidney disease, where baseline tubular sodium wasting raises FENa regardless of the acute insult.
- The original derivation (Espinel 1976) was in a small, selected, oliguric cohort that excluded obstruction, glomerulonephritis, CKD, and diuretic use; applying FENa outside those bounds reduces its accuracy.
- FENa is an adjunct, not a diagnosis. Always interpret it with the history, volume status, urine microscopy, and the trajectory of renal function.
FENa (%) = (Urine sodium x Plasma creatinine) / (Plasma sodium x Urine creatinine) x 100. Sodium values in mmol/L; the two creatinine values must share the same unit (here mg/dL), and that unit cancels.Frequently asked
What FENa value separates prerenal from intrinsic kidney injury?
In oliguric acute kidney injury, a FENa below 1% suggests prerenal azotemia and a value above 2% suggests intrinsic injury such as acute tubular necrosis. Values between 1% and 2% are indeterminate and need clinical correlation.
Why is FENa unreliable in patients taking diuretics?
Loop and thiazide diuretics block tubular sodium reabsorption, so they raise urine sodium and FENa even when the patient is volume-depleted and prerenal. In that situation the fractional excretion of urea is preferred: a FEUrea below about 35% supports prerenal azotemia (Carvounis et al. 2002).
Can FENa be below 1% in intrinsic kidney disease?
Yes. Contrast-induced nephropathy, early or acute glomerulonephritis, rhabdomyolysis, and hepatorenal syndrome can all produce a FENa under 1% despite genuine intrinsic renal involvement, so a low value is suggestive of prerenal disease but not specific.
A score is a start. The product is asked.
Calculators give a number. When the patient in front of you needs the reasoning behind it, with the sources, the product is what does the looking-up.
Medical AI returns evidence-grounded answers backed by real citations. It is a reference tool, and these terms describe how it should and should not be used.
01 Educational purpose
Medical AI is an information and reference tool intended for educational use only. The answers it returns are not medical advice, diagnosis, or treatment. Always consult a qualified doctor or healthcare professional with any question concerning a medical condition.
02 Professional use
Medical AI is designed for use by practicing clinicians. It is not intended for direct patient use and is not a substitute for professional clinical judgment. Apply your own training and current guidelines to every decision an answer informs.
03 Privacy and data
We do not collect, store, or process personally identifiable patient information (PHI or PII). Do not enter names, dates of birth, medical record numbers, or any other patient identifiers into the composer.
04 Information currency
Medical knowledge evolves rapidly. Citations carry their publication date, so consult the primary source and the most recent clinical guideline before acting on anything material.