Loading...
Printed on 7/19/2026
For informational purposes only. This is not medical advice.
FEUrea estimates the fraction of filtered urea excreted in urine. It is often used in acute kidney injury when patients are receiving diuretics, because FEUrea is generally less affected by natriuretic therapy than FENa.
Formula: FEUrea (%) = (Urine Urea x Serum Cr) / (Serum Urea x Urine Cr) x 100.
Save your results with a free account
Keep a history of calculations, favorite tools, and access your dashboard anytime.
Obtain a spot urine and a simultaneous blood sample to measure urine urea nitrogen (BUN), serum urea nitrogen (BUN), urine creatinine, and serum creatinine. No timed collection is required — a spot sample is sufficient.
FEUrea (%) = (urine BUN × serum creatinine) / (serum BUN × urine creatinine) × 100. This calculates the fraction of filtered urea that is excreted in urine, expressed as a percentage.
FEUrea <35% indicates avid urea reabsorption consistent with renal hypoperfusion (pre-renal AKI). FEUrea >50% suggests tubular damage (ATN) with impaired reabsorption. The range 35–50% is indeterminate. FEUrea is more reliable than FENa in diuretic-treated patients.
Nephrologists, hospitalists
FEUrea is the preferred alternative to FENa when a patient with AKI is on loop or thiazide diuretics. Diuretics dramatically increase urinary sodium excretion, falsely elevating FENa and suggesting intrinsic AKI even in purely pre-renal states. FEUrea avoids this confound.
Cardiologists, nephrologists
Decompensated heart failure patients are often on loop diuretics and develop AKI from renal hypoperfusion. FENa is unreliable in this group. FEUrea <35% supports pre-renal (cardiorenal syndrome type 1), while >50% suggests coexisting ATN from renal congestion or ischemia.
Internal medicine, nephrology
Patients on chronic thiazide or loop diuretics for hypertension, cirrhosis, or edema frequently develop AKI from dehydration or infection. FEUrea provides a diuretic-resistant assessment of tubular function to guide fluid resuscitation decisions.
Emergency physicians, intensivists
Beyond diuretics, FENa can be falsely low or high in many conditions (contrast nephropathy, myoglobinuria, early obstruction). In these settings, FEUrea may provide complementary information when combined with clinical context, urinalysis, and renal ultrasound.
Hospitalists, internal medicine residents
FEUrea requires only a spot urine and blood sample, results are available within hours, and the calculation is simple. It provides an objective data point to guide initial AKI management — fluid challenge vs. watchful waiting — in diuretic-treated patients.
Loop diuretics (furosemide, bumetanide) and thiazides increase tubular sodium excretion, falsely raising FENa above 1% even in pure pre-renal states. FEUrea is largely unaffected because urea reabsorption is passive and not directly driven by the sodium transporters blocked by diuretics.
Unlike sodium (which is actively reabsorbed), tubular urea transport is largely passive. This means diuretic-induced natriuresis does not directly alter urea reabsorption in the same way. FEUrea therefore better reflects the overall tubular reabsorptive capacity independent of diuretic effect.
High dietary protein intake increases urea production beyond kidney excretion, raising serum BUN. GI bleeding provides a protein load from digested blood, also raising BUN. Corticosteroids are catabolic and increase urea generation. In these settings, high serum BUN relative to urine BUN can make FEUrea appear falsely low (suggesting pre-renal) even in ATN.
The original Carvounis et al. (2002) study found FEUrea <35% had 85% sensitivity and 92% specificity for pre-renal AKI in diuretic-treated patients. Subsequent studies have generally supported its utility, though performance varies by clinical context and patient population.
FEUrea is one data point, not a standalone diagnosis. Combine with: urine output trends, blood pressure and volume status exam, response to fluid challenge, urinalysis microscopy (muddy brown casts = ATN), renal ultrasound (obstruction), and medication review (nephrotoxins).
Patients with CKD have impaired tubular reabsorptive capacity at baseline. Even in a pre-renal state, their tubules may not concentrate urine as effectively, leading to a higher FEUrea than expected for pure pre-renal. Interpret in the context of baseline renal function.
In patients NOT on diuretics, FENa <1% is a well-validated predictor of pre-renal AKI with high sensitivity and specificity. FEUrea should be used as the primary test only when diuretics are present. When neither drug is given, both FENa and FEUrea can be used together for complementary assessment.
Urine osmolality >500 mOsm/kg strongly supports pre-renal physiology and tubular concentrating ability. Combined with FEUrea <35%, this provides a more robust picture of pre-renal AKI. In ATN, urine osmolality is typically <350 mOsm/kg due to tubular injury impairing concentrating ability.
A BUN:creatinine ratio >20 is an additional marker of pre-renal physiology (or upper GI bleeding). Combining the BUN:Cr ratio with FEUrea strengthens the pre-renal diagnosis. However, GI bleeding can elevate BUN:Cr even in ATN, so always verify the clinical story.
In severe heart failure with intense neurohormonal activation (RAAS, ADH), avid sodium retention can overcome diuretic natriuresis, resulting in low FENa despite diuretic use. This makes FEUrea particularly valuable in this subgroup, though even FEUrea can be borderline in advanced cardiorenal syndrome.
Fractional excretion of urea was proposed as an alternative to FENa for patients on diuretics by Carvounis et al. (Am J Kidney Dis 2002), who showed FEUrea <35% had 85% sensitivity and 92% specificity for pre-renal AKI in diuretic-treated patients. Subsequent studies have validated its utility in decompensated heart failure patients (Steinhausen et al., NDT 2008). FEUrea limitations in high-protein states are reviewed in Diskin (NDT 2010).
Lower FEUrea values are more consistent with pre-renal kidney hypoperfusion, while higher values suggest intrinsic renal tubular dysfunction in the proper clinical setting.
Use FEUrea during AKI evaluation when the patient is on loop or thiazide diuretics and FENa may be misleading.
Thresholds are not absolute and performance varies by population and timing. FEUrea should be interpreted with full clinical context rather than used as a standalone diagnostic test.
Disclaimer: This tool is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about your health.
April 21, 2026 · trust-baseline
Clinical trust metadata enabled for this tool page with structured review/version fields.
Calculate the Fractional Excretion of Sodium (FENa) to differentiate pre-renal azotemia (FENa <1%) from intrinsic renal disease such as ATN (FENa >2%) in acute kidney injury.
OpenNephrologyCalculate the BUN/Creatinine ratio to distinguish pre-renal from intrinsic acute kidney injury. Normal ratio 10–20. Ratio >20 suggests pre-renal azotemia; <10 suggests intrinsic renal disease.
OpenClinicalCalculate eGFR with the CKD-EPI 2021 race-free formula to estimate kidney function and CKD stage from serum creatinine, age, and sex.
Open