Prerenal vs Intrinsic AKI Interpreter
Prerenal vs Intrinsic AKI Interpreter
Is an acute kidney injury prerenal or acute tubular necrosis? Enter the FENa — or the FEUrea if a diuretic has been given — with the urine sodium, urine osmolality and the urine sediment. The page reads them together and says plainly when the classic cut-offs do not apply: chronic kidney disease, sepsis, contrast, obstruction, glomerulonephritis, and any patient who is not oliguric.
Is this AKI prerenal or tubular injury?
FENa or FEUrea + urine + sediment → prerenal or ATNAn 80-year-old with three days of diarrhoea; creatinine 2.4 mg/dL from 1.0. Oliguric, no diuretic, no CKD. FENa 0.4%, urine sodium 12 mmol/L, urine osmolality 610 mOsm/kg, bland sediment.
The indices and where they come from
FEUrea (%) = (urine urea × plasma creatinine) ÷ (plasma urea × urine creatinine) × 100 — prerenal 35% or less, ATN above 50%
Miller 1978, in acute oliguria: prerenal = urine osmolality above 500, urine sodium below 20; ATN = osmolality below 350, sodium above 40
- FENa
- use when no diuretic has been given; see the FENa calculator
- FEUrea
- use after a loop or thiazide diuretic; see the FEUrea calculator
- oliguric
- the population the cut-offs were derived in
Worked example
An 80-year-old with three days of diarrhoea; creatinine 2.4 mg/dL from 1.0. Oliguric, no diuretic, no CKD. FENa 0.4%, urine sodium 12 mmol/L, urine osmolality 610 mOsm/kg, bland sediment.
No obstruction concern, no active or granular sediment, no sepsis or contrast
No diuretic → read the FENa: 0.4% is below 1%
Urine sodium below 20 and osmolality above 500 agree with it
Oliguric → the setting the cut-offs were built in → prerenal pattern; rehydrate and expect recovery within a day or two
When a low FENa does not mean prerenal, and a high one does not mean ATN
| Setting | What happens | Source |
|---|---|---|
| Diuretic given | FENa rises whatever the volume state; only 48% of prerenal patients on diuretics had FENa ≤ 1% | Carvounis 2002 |
| Chronic kidney disease | Resting FENa is above 1% because fewer nephrons excrete the same sodium intake | Nguyen 2009 |
| Iodinated contrast | Contrast nephropathy can show FENa below 1% | Fang 1980 |
| Sepsis | Urinary indices unreliable for diagnosis | Bagshaw 2006 |
| Obstruction, glomerulonephritis, allograft rejection, some drugs, some ATN | FENa below 1% reported | Zarich 1985 |
| Not oliguric | Lower specificity for prerenal AKI | Miller 1978 |
Where the 1% comes from, and where it fails
The fractional excretion of sodium asks how much of the sodium filtered by the glomeruli ends up in the urine. When the kidney is under-perfused but its tubules are intact, it reabsorbs sodium avidly and FENa falls below 1%. When the tubules are injured, as in acute tubular necrosis, they cannot, and FENa rises. That logic is sound, but the 1% figure was derived in a particular population: Espinel’s 1976 study and Miller’s 1978 prospective study were both of oliguric acute renal failure. Miller’s abstract says so directly, and adds that a significant number of oliguric patients do not fall within the guidelines at all.
Outside that population the test degrades. A loop or thiazide diuretic makes the kidney excrete sodium regardless of volume, so fewer than half of prerenal patients who had received one kept a FENa at or below 1%; urea handling is barely touched by diuretics, which is why the fractional excretion of urea, with prerenal at 35% or less, replaced it in that setting (FEUrea calculator). In chronic kidney disease the surviving nephrons must excrete the whole day’s sodium between them, so the resting FENa is already above 1% — about 2.5% at a GFR of 30 on an ordinary diet — and a value of 1.5% can be appropriate retention. In the other direction, contrast nephropathy, early obstruction, glomerulonephritis, transplant rejection and sepsis have all been reported with a FENa below 1% despite intrinsic injury.
The urine sediment often settles what the numbers cannot. Granular (muddy brown) casts and tubular epithelial cells point to ATN, red cell casts to glomerular disease, and a bland sediment to a prerenal cause. Stage the injury itself with the KDIGO AKI stage calculator, and calculate the indices with the FENa calculator. This page supports clinical judgement and does not replace it.
Frequently asked questions
What FENa means prerenal AKI?
Below 1% in an oliguric patient who has not had a diuretic. Above 1% suggests acute tubular necrosis. The cut-off comes from oliguric patients and is less reliable in others.
When should FEUrea be used instead of FENa?
When a loop or thiazide diuretic has been given. FEUrea of 35% or less suggests prerenal AKI and above 50% suggests ATN; urea handling is largely unaffected by diuretics.
Why is FENa unreliable in chronic kidney disease?
With fewer nephrons, each must excrete more of its filtered sodium to match intake, so the baseline FENa is already above 1%. A FENa above 1% in CKD does not prove tubular injury.
Can a FENa below 1% still be intrinsic kidney injury?
Yes: contrast nephropathy, early obstruction, glomerulonephritis, transplant rejection and sepsis have all been described with a low FENa.
Related calculators
References
- Miller TR, Anderson RJ, Linas SL, et al. Urinary diagnostic indices in acute renal failure: a prospective study. Ann Intern Med. 1978;89(1):47–50.
- Espinel CH. The FENa test: use in the differential diagnosis of acute renal failure. JAMA. 1976;236(6):579–581.
- Carvounis CP, Nisar S, Guro-Razuman S. Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney Int. 2002;62(6):2223–2229.
- Zarich S, Fang LS, Diamond JR. Fractional excretion of sodium: exceptions to its diagnostic value. Arch Intern Med. 1985;145(1):108–112.
- Fang LS, Sirota RA, Ebert TH, Lichtenstein NS. Low fractional excretion of sodium with contrast media-induced acute renal failure. Arch Intern Med. 1980;140(4):531–533.
- Nguyen MT, Maynard SE, Kimmel PL. Misapplications of commonly used kidney equations: renal physiology in practice. Clin J Am Soc Nephrol. 2009;4(3):528–534.
- Bagshaw SM, Langenberg C, Bellomo R. Urinary biochemistry and microscopy in septic acute renal failure: a systematic review. Am J Kidney Dis. 2006;48(5):695–705.
- Perazella MA, Coca SG, Kanbay M, Brewster UC, Parikh CR. Diagnostic value of urine microscopy for differential diagnosis of acute kidney injury in hospitalized patients. Clin J Am Soc Nephrol. 2008;3(6):1615–1619.
- Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2(1):1–138.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.