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The Fractional Excretion of Urea (FEUrea) Calculator determines the percentage of filtered urea that is excreted in the urine. FEUrea is particularly valuable for evaluating acute kidney injury in patients who have received diuretics, a situation where the more commonly used FENa becomes unreliable. Because diuretics primarily affect sodium handling without significantly altering urea reabsorption, FEUrea maintains its diagnostic accuracy in the presence of diuretic therapy.
FEUrea is calculated using the same general formula as FENa but substituting urea for sodium: FEUrea (%) = (Urine Urea x Plasma Creatinine) / (Plasma BUN x Urine Creatinine) x 100. A FEUrea below 35% suggests pre-renal azotemia, indicating that the kidney is maximally reabsorbing urea in response to reduced perfusion. A FEUrea above 50% suggests intrinsic renal disease with impaired tubular urea reabsorption. Values between 35% and 50% are indeterminate.
The physiological basis for FEUrea interpretation parallels that of FENa. In pre-renal states, reduced renal blood flow and increased antidiuretic hormone (ADH) activity enhance water and urea reabsorption in the collecting duct. Urea reabsorption is mediated by urea transporters (UT-A1 and UT-A3) in the inner medullary collecting duct, which are upregulated by ADH and function independently of the sodium transport mechanisms targeted by diuretics. This is why FEUrea remains accurate in diuretic-treated patients while FENa becomes falsely elevated.
The clinical validation of FEUrea was established in a pivotal study by Carvounis and colleagues in 2002, which compared FENa and FEUrea in 102 patients with AKI, including a subgroup receiving diuretics. In diuretic-treated patients, FENa correctly identified pre-renal azotemia only 48% of the time, while FEUrea maintained 90% sensitivity and 83% specificity for pre-renal azotemia. This finding established FEUrea as the preferred test for AKI evaluation in diuretic-exposed patients.
FEUrea has limitations as well. It may be affected by very high or low protein intake (which alters urea production), liver disease (impaired urea synthesis), and osmotic diuretics (which can increase urea excretion). In patients with complete anuria, urinary indices cannot be obtained. In CKD with chronically impaired concentrating ability, baseline FEUrea may be elevated, complicating interpretation of acute changes. Despite these limitations, FEUrea fills a critical diagnostic gap in the common clinical scenario of AKI evaluation in patients already receiving diuretics.
In practice, FEUrea and FENa are often obtained simultaneously as complementary tests. When both results are concordant (both suggesting pre-renal or both suggesting intrinsic renal), diagnostic confidence is high. When results are discordant, diuretic exposure is the most common explanation, and FEUrea should be given priority. Integrating these laboratory findings with clinical assessment, response to volume resuscitation, and serial creatinine measurements provides the most complete picture for guiding AKI management.
FEUrea is calculated as (Urine Urea x Plasma Creatinine) / (Plasma BUN x Urine Creatinine) x 100. This ratio normalizes urea excretion to creatinine clearance. Values below 35% indicate enhanced urea reabsorption (pre-renal), while above 50% indicates impaired tubular function (intrinsic renal). Unlike FENa, FEUrea remains reliable after diuretic administration.
FEUrea below 35% suggests pre-renal azotemia — the kidney is appropriately retaining urea in response to hypovolemia or hypoperfusion. FEUrea above 50% suggests intrinsic renal disease (ATN). FEUrea 35-50% is indeterminate. FEUrea is most valuable when diuretics have been given and FENa is unreliable. Obtain samples before additional interventions when possible.
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FEUrea of 40% is in the indeterminate zone. Clinical context, response to fluids, and serial creatinine should guide management.
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FEUrea borderline at 48%, approaching the intrinsic threshold. Combined with clinical findings (granular casts, non-response to fluids), ATN is likely.
Use FEUrea when the patient has received diuretics (loop, thiazide, or potassium-sparing), as diuretics artificially increase urinary sodium and make FENa unreliable. FEUrea is unaffected by most diuretics because urea reabsorption occurs through ADH-dependent urea transporters, not sodium transporters.
In healthy individuals with normal kidney function and hydration, FEUrea is typically 50-65%. During pre-renal states, it drops below 35% as the kidney enhances urea reabsorption. In intrinsic renal disease, tubular urea reabsorption is impaired and FEUrea exceeds 50%.
ADH (vasopressin) upregulates urea transporter expression in the inner medullary collecting duct, increasing urea reabsorption. In pre-renal states where ADH levels are elevated, this mechanism maximizes urea retention, lowering FEUrea. This ADH-dependent pathway is independent of sodium transport.
FEUrea below 35% suggests pre-renal azotemia. FEUrea above 50% suggests intrinsic renal disease. FEUrea between 35% and 50% is indeterminate and requires additional clinical information for diagnosis. These thresholds were established from the Carvounis validation study.
FEUrea is less reliable in CKD patients because chronic tubular damage impairs baseline urea reabsorption, resulting in higher FEUrea at baseline. An acute increase in FEUrea from the patient's known baseline may suggest intrinsic AKI superimposed on CKD.
Yes. High protein intake increases urea production and can increase FEUrea. Very low protein intake reduces urea production. These effects are usually modest and unlikely to change the clinical interpretation across the diagnostic thresholds, but should be considered in extreme dietary situations.
A spot urine sample obtained simultaneously with a blood sample is sufficient. No timed collection is needed. Send the urine for urea nitrogen (or BUN equivalent) and creatinine, along with serum BUN and creatinine. Results are typically available within hours.
Yes. Osmotic diuretics (mannitol, glucose in uncontrolled diabetes) can increase urea excretion by increasing water flow through the nephron, which drags urea with it. In these situations, both FENa and FEUrea may be unreliable, and clinical judgment becomes paramount.
FEUrea is not inherently superior — it is complementary. In patients without diuretic exposure, FENa and FEUrea perform similarly. FEUrea's advantage is specifically in diuretic-treated patients where FENa loses diagnostic accuracy. Using both tests together provides the most reliable information.
Acute interstitial nephritis (AIN) can have variable FEUrea values. Some cases show low FEUrea (mimicking pre-renal) because the inflammatory process does not always destroy tubular function early in the disease. Clinical features (rash, eosinophilia, medication exposure) and renal biopsy may be needed for diagnosis.
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