Calculate FEUrea to differentiate prerenal from intrinsic AKI in patients on diuretics. Includes FEUrea vs FENa comparison, AKI diagnostic indices, and clinical interpretation.
The Fractional Excretion of Urea (FEUrea) Calculator estimates what percentage of filtered urea is excreted in the urine. It is mainly used as a bedside AKI aid when diuretics make FENa harder to interpret, because loop and thiazide diuretics directly change urinary sodium handling but have less direct effect on the urea-based calculation.
This page converts the entered urea and creatinine measurements into a common unit system, applies the standard FEUrea formula, and places the result into the usual prerenal, indeterminate, or intrinsic-renal bands. It also keeps the FEUrea-versus-FENa context visible so the result is not read in isolation.
The output is still only one part of AKI assessment. Volume status, urine sediment, medication exposure, obstruction, CKD, sepsis, and the rest of the renal workup can change what the number means in practice.
When AKI is being evaluated in a patient on diuretics, the usual sodium-based indices are harder to interpret. This calculator keeps the urea and creatinine inputs together, applies the same fractional-excretion structure every time, and makes the prerenal-versus-intrinsic split easier to review alongside the rest of the urine studies already being collected.
FEUrea (%) = (UUrea × PCr) / (PUrea × UCr) × 100 Where: • UUrea = Urine urea (mg/dL) • PUrea = Plasma urea (mg/dL) • UCr = Urine creatinine (mg/dL) • PCr = Plasma creatinine (mg/dL) Conversions: • BUN → Urea: × 2.14 • Urea mmol/L → mg/dL: × 6.006 • Creatinine µmol/L → mg/dL: ÷ 88.42 Interpretation: • FEUrea < 35%: Prerenal • FEUrea 35–50%: Indeterminate • FEUrea > 50%: Intrinsic (ATN)
Result: FEUrea = 46.9% — Indeterminate, but trending toward intrinsic
FEUrea = (600 × 2.5)/(80 × 40) × 100 = 1500/3200 × 100 = 46.9%. This falls in the indeterminate zone (35–50%). Additional information is needed: urine microscopy (muddy brown casts → ATN), clinical trajectory (improving with fluids → prerenal), and urine osmolality. If the patient is on diuretics, FEUrea is more reliable than FENa for this assessment.
FEUrea is most often reviewed when a patient has already received diuretics and the usual sodium-based indices become harder to interpret. The calculation does not solve AKI by itself, but it can add another structured data point when volume status, urine sediment, and medication exposure are all being reviewed together.
CKD, sepsis, gastrointestinal bleeding, low urea production, urine-flow changes, and mixed etiologies can all make FEUrea less decisive. The overlap zone is common, which is why the page keeps the indeterminate range visible instead of forcing a binary answer.
Urine microscopy, the clinical course, ultrasound when obstruction is possible, and repeat chemistry often do more to sort out AKI than one urinary index alone. FEUrea is most useful when it helps organize that broader picture rather than replacing it.
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This page calculates fractional excretion of urea as "(urine urea × plasma creatinine) / (plasma urea × urine creatinine) × 100" after normalizing the entered urea and creatinine measurements to compatible units. It then groups the result into the conventional bedside interpretation bands of less than 35%, 35% to 50%, and greater than 50%, while showing the surrounding AKI context and the FENa comparison on the same page.
The result is intended mainly for AKI assessment when diuretic exposure makes sodium-based indices harder to interpret. It is not a stand-alone diagnosis, and CKD, sepsis, gastrointestinal bleeding, low urea production, urine sediment, obstruction, and the overall clinical picture can all change how much weight the FEUrea number deserves.
Loop and thiazide diuretics directly change urinary sodium handling, which can push FENa upward even when the patient is still sodium avid. FEUrea is often less distorted by that effect, so it can be a helpful additional clue after diuretics have been given. It is still not perfect, and the number should be read alongside urine sediment, volume status, and the rest of the AKI workup.
FEUrea has several limitations: 1) Less extensively validated than FENa (fewer studies), 2) Overlap zone (35–50%) can be wide, 3) High-protein diet or GI bleeding can increase urea production independently, 4) CKD alters baseline urea handling, 5) Severe liver disease reduces urea production, 6) It doesn't account for the same intrinsic-renal exceptions as FENa (contrast nephropathy, rhabdomyolysis). Like FENa, it should be one part of the AKI workup, not the sole determinant.
Yes — when both are available, concordant results strengthen the diagnosis. If FENa and FEUrea both point to prerenal (<1%, <35%), prerenal is very likely. If FENa is elevated (>1%) but FEUrea is low (<35%) in a patient on diuretics, prerenal is likely (diuretics explain the elevated FENa). If both are elevated (FENa >2%, FEUrea >50%), intrinsic AKI is strongly suggested. Discordant results in a patient NOT on diuretics require additional workup.
BUN (Blood Urea Nitrogen) measures only the nitrogen portion of the urea molecule, while "urea" measures the entire molecule. The conversion factor is: Urea = BUN × 2.14 (molecular weight ratio: 60/28). In the US, labs typically report BUN (mg/dL), while international labs often report urea (mmol/L or mg/dL). This distinction matters for calculations — using BUN values in a formula expecting urea (or vice versa) will give incorrect results. Our calculator handles the conversion automatically.
Renal biopsy is considered when: 1) AKI doesn't fit a clear pattern (not obviously prerenal, ATN, or obstructive), 2) Features suggest glomerulonephritis (hematuria, proteinuria, red cell casts, low complement), 3) AKI persists despite appropriate management (unexplained persistent AKI beyond 3–4 weeks), 4) Systemic disease workup is positive (ANCA, anti-GBM, ANA), 5) Drug-induced interstitial nephritis is suspected but steroids are being considered. Biopsy provides definitive histological diagnosis and guides specific therapy.
Novel biomarkers (NGAL, KIM-1, IL-18, TIMP-2×IGFBP7) detect tubular injury hours before creatinine rises, whereas FEUrea (like FENa) requires creatinine elevation to calculate. The biomarkers identify "subclinical AKI" — tubular damage before it manifests as decreased GFR. TIMP-2×IGFBP7 (NephroCheck) is FDA-cleared for AKI risk assessment in ICU patients. However, these biomarkers complement rather than replace traditional indices: they detect injury early, while FENa/FEUrea help classify the mechanism after AKI is established.