FEUrea Calculator: Acute Kidney Injury Cause Differentiation
The FEUrea calculator computes the fractional excretion of urea from serum and urine creatinine and urea values. It is used at bedside to differentiate prerenal azotemia from intrinsic renal injury, and unlike FENa it remains reliable in patients receiving loop diuretics. Enter your lab values and get an instant result with a clinical interpretation.
Formula
Worked example
A patient with AKI on furosemide has serum BUN 28 mg/dL, serum creatinine 2.5 mg/dL, urine urea 180 mg/dL, and urine creatinine 80 mg/dL. FEUrea = (180 x 2.5) / (28 x 80) x 100 = 450 / 2240 x 100 = 20.1%. This borderline result is in the lower prerenal zone and, given diuretic use where FENa would be unreliable, suggests prerenal physiology with careful fluid management indicated.
What is FEUrea and why is it used?
The fractional excretion of urea (FEUrea) measures what fraction of the urea filtered by the glomerulus is ultimately excreted in the urine. In a healthy person with normal renal perfusion, the tubules reabsorb about 40-60% of filtered urea passively alongside water in the proximal tubule and descending loop of Henle. When renal perfusion falls - as in dehydration, heart failure, or sepsis-related hypotension - the kidney compensates by reabsorbing more urea and water, driving FEUrea below 35%. When the tubules themselves are damaged (acute tubular necrosis, nephrotoxin exposure), urea reabsorption is impaired and FEUrea rises above 50%. This makes FEUrea a direct window into tubular function rather than just filtration rate. Its key clinical advantage is that loop and thiazide diuretics, which force urinary sodium excretion and invalidate fractional excretion of sodium (FENa), have little effect on urea reabsorption. FEUrea therefore remains the preferred test for AKI differentiation in any patient receiving diuretic therapy.
How to collect and interpret the values
FEUrea requires four simultaneous measurements: serum creatinine, serum urea (reported as BUN in the United States), urine creatinine, and urine urea from a spot urine sample. Blood and urine ideally should be collected within minutes of each other, and samples should be processed within two hours to avoid urea degradation by urease-producing bacteria. The result is a percentage. Below 35% points toward prerenal azotemia; above 50% points toward intrinsic renal injury such as ATN. The 35-50% range is indeterminate and should be interpreted alongside clinical volume status, urine microscopy (looking for granular casts that signal ATN), urine sodium, and the trajectory of creatinine. In sepsis-related AKI, FEUrea can be misleadingly low even when there is true tubular injury - a recognised limitation. FEUrea is also less reliable in advanced chronic kidney disease (CKD stages 4-5), post-obstructive AKI, contrast nephropathy, rhabdomyolysis, and patients receiving glucocorticoids or osmotic diuretics.
FEUrea vs FENa: which should I use?
Fractional excretion of sodium (FENa) was the original bedside tubular function test. A FENa below 1% suggests prerenal azotemia; above 2% suggests ATN. However, FENa fails in any clinical situation that alters urinary sodium independently of tubular function, most commonly loop diuretics and thiazides. A patient with genuine volume depletion who received furosemide will have a falsely elevated FENa, potentially misclassified as intrinsic AKI. Because urea reabsorption is passive and follows water rather than sodium-potassium pumps, it is unaffected by these drugs. The landmark 2002 study by Carvounis et al. showed FEUrea had 85% sensitivity and 92% specificity for prerenal AKI and outperformed FENa in patients on diuretics. Neither test is perfect: both should always be paired with the clinical picture. For a patient who has not received diuretics and has straightforward clinical findings, FENa and FEUrea give concordant information; reserve FEUrea as the primary test when diuretics have been given or FENa seems inconsistent with the clinical assessment.
Limitations and when not to use FEUrea
FEUrea has well-documented limitations. In sepsis-associated AKI, cytokine-driven increases in ADH and urea transporter activity can keep FEUrea low despite significant tubular injury, creating false-negative results. In advanced CKD, chronically altered tubular dynamics make the standard cut-offs unreliable. Post-obstructive AKI and contrast nephropathy can produce low FEUrea even with tubular damage. Patients taking glucocorticoids have increased hepatic urea production and altered urea handling that skews results. Gastrointestinal bleeding raises serum BUN disproportionately, artificially lowering the calculated FEUrea. Osmotic diuretics and uncontrolled hyperglycemia also compromise the test. In any of these situations, FEUrea should supplement rather than replace a thorough clinical assessment including volume history, blood pressure trends, urine microscopy, kidney ultrasound, and selective use of kidney biomarkers such as NGAL or KIM-1 when available.
FEUrea interpretation thresholds
| FEUrea (%) | Interpretation | Probable cause |
|---|---|---|
| < 20 | Strongly prerenal | Severe volume depletion or reduced perfusion |
| 20-34 | Prerenal likely | Mild-moderate volume depletion or reduced renal perfusion |
| 35-50 | Indeterminate zone | Requires clinical context and additional tests |
| > 50 | Intrinsic renal disease likely | Acute tubular necrosis or other tubular injury |
Standard clinical cut-offs for interpreting fractional excretion of urea in acute kidney injury. Values apply to adults with AKI, not to baseline CKD.
Frequently asked questions
What is a normal FEUrea?
There is no single "normal" FEUrea because the value is only meaningful in the context of acute kidney injury. In people without AKI, FEUrea typically falls between 40% and 65%, reflecting routine urea handling. In AKI, the diagnostic cut-offs are below 35% for prerenal and above 50% for intrinsic renal disease.
Why is FEUrea better than FENa on diuretics?
Loop and thiazide diuretics block tubular sodium reabsorption and raise urinary sodium independently of renal perfusion. This falsely elevates FENa and can make a prerenal patient look like they have ATN. Because urea reabsorption is passive and driven by water movement rather than active sodium transport, diuretics do not substantially affect FEUrea, keeping it interpretable even after furosemide or hydrochlorothiazide.
Can I use a random (spot) urine sample?
Yes. FEUrea uses the ratio of urea to creatinine concentrations in both blood and urine, so a random spot urine collection is adequate. A 24-hour collection is not needed. The key requirement is that blood and urine samples are obtained at approximately the same time and processed promptly, ideally within two hours, to prevent urea degradation.
What does the 35-50% range mean?
The 35-50% zone is clinically indeterminate: neither prerenal nor intrinsic AKI can be confidently diagnosed from FEUrea alone. In this range, the test should be supplemented with urine microscopy (granular or muddy-brown casts support ATN), urine sodium concentration, clinical assessment of volume status, and the rate of change in serum creatinine. Nephrologist input is often valuable when FEUrea is indeterminate.
Is FEUrea reliable in chronic kidney disease?
Not reliably. Patients with CKD stages 4 and 5 have chronic alterations in urea and creatinine handling that shift the expected values away from the standard cut-offs. FEUrea should be used with caution in advanced CKD, and results interpreted in the context of the patient's baseline kidney function. Some centres use the change from the patient's known baseline rather than absolute thresholds.
What are the units for FEUrea?
FEUrea is expressed as a percentage (%). The individual lab values can be in conventional units (mg/dL for urea/BUN and creatinine) or SI units (mmol/L for urea, umol/L for creatinine). This calculator accepts both and converts internally before computing the ratio, so the final percentage is the same regardless of which unit system you use.
Sources
- Carvounis CP, Nisar S, Guro-Razuman S. Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney International. 2002.
- Perazella MA, Coca SG. Traditional urinary biomarkers in the assessment of hospital-acquired AKI. Clinical Journal of the American Society of Nephrology. 2012.