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 computes the percentage of filtered urea excreted in the urine, specifically designed for differentiating prerenal from intrinsic acute kidney injury (AKI) in patients receiving diuretics. While FENa is the standard first-line test, diuretics (loop diuretics, thiazides) invalidate FENa by directly increasing urinary sodium excretion. FEUrea was developed by Carvounis et al. (2002) as a diuretic-resistant alternative.
Urea reabsorption occurs primarily in the medullary collecting duct (via UT-A1 and UT-A3 transporters), driven by ADH and medullary concentration gradients. In prerenal states, enhanced ADH activity and slow tubular flow increase urea reabsorption, yielding FEUrea <35%. In intrinsic AKI (ATN), tubular damage disrupts the medullary concentration gradient, reducing urea reabsorption and elevating FEUrea above 50%. Critically, loop diuretics act at the thick ascending limb of Henle, which is not the primary site of urea transport — this is why FEUrea maintains its diagnostic utility when diuretics are on board.
The calculator supports multiple unit systems (urea in mg/dL, BUN in mg/dL, urea in mmol/L) with automatic conversion, and provides a comprehensive comparison of FEUrea versus FENa with clinical decision support for the AKI workup.
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.
Urea is freely filtered at the glomerulus, then undergoes complex handling: 50% is reabsorbed in the proximal tubule (passive, follows water), secreted into the thin descending limb of Henle (urea recycling), and 40–60% is reabsorbed in the medullary collecting duct via UT transporters (ADH-dependent). In prerenal states, enhanced ADH activity and slow tubular flow increase collecting duct urea reabsorption, concentrating the medulla and lowering FEUrea. In ATN, dysfunction of these transporters raises FEUrea.
Carvounis et al. (2002) first validated FEUrea in 102 AKI patients, showing FEUrea <35% had 85% sensitivity and 92% specificity for prerenal AKI, compared to FENa which had only 48% sensitivity in diuretic-treated patients. Subsequent studies have generally confirmed its utility, though diagnostic performance varies by population. A meta-analysis by Diskin et al. suggested that FEUrea cutoffs may need adjustment in CKD populations and elderly patients.
In clinical practice: 1) Establish AKI diagnosis (KDIGO criteria), 2) Assess for obstruction (ultrasound), 3) Review medications and exposures, 4) Check FENa (if no diuretics) or FEUrea (if on diuretics), 5) Send urine microscopy (always), 6) Consider novel biomarkers in ICU settings. The combination of clinical assessment + urinary indices + microscopy correctly classifies >90% of AKI cases. Those that remain unclear may warrant nephrology consultation and possible biopsy.
Loop diuretics (furosemide, bumetanide) block the Na-K-2Cl cotransporter in the thick ascending limb of Henle, directly increasing urinary sodium excretion. This artificially elevates FENa, potentially making a prerenal patient appear to have intrinsic AKI. Urea, however, is primarily reabsorbed in the collecting duct (not the thick ascending limb), so loop diuretics don't significantly affect urea handling. FEUrea therefore maintains its diagnostic accuracy regardless of diuretic status.
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.