Fractional Excretion of Urea (FEUrea) Calculator
Differentiate prerenal from intrinsic acute kidney injury in patients receiving diuretics — where the standard FeNa is unreliable. FEUrea is unaffected by loop and thiazide diuretics and provides a more accurate assessment of tubular function in this common clinical scenario.
Calculate FEUrea & FeNa
Enter plasma and urine urea (BUN) and creatinine to calculate FEUrea. Optionally, enter plasma and urine sodium to also calculate FeNa for comparison. FEUrea is the preferred index in patients on diuretics. For patients not on diuretics, see also the FeNa Calculator.
Loop and thiazide diuretics directly block tubular sodium reabsorption, which falsely elevates FeNa — a patient with genuinely prerenal AKI may appear to have intrinsic disease. Urea reabsorption in the proximal tubule is coupled to passive water movement and is not significantly affected by diuretics, making FEUrea a more reliable index in this very common clinical scenario.
Understanding Fractional Excretion of Urea
The fractional excretion of urea (FEUrea) measures the percentage of filtered urea that is excreted in the urine. Urea is freely filtered at the glomerulus, then passively reabsorbed in the proximal tubule and inner medullary collecting duct — driven primarily by water reabsorption mediated by ADH. In prerenal states, enhanced proximal sodium and water reabsorption increases passive urea reabsorption, resulting in a low FEUrea (<35%). When the tubules are damaged, this passive reabsorption is disrupted and FEUrea rises above 50%.
Carvounis and colleagues validated FEUrea in 2002 by studying 102 patients with AKI, including 50 who were receiving diuretics. They demonstrated that FEUrea retained its ability to differentiate prerenal from intrinsic AKI in diuretic-treated patients with a sensitivity of 85% and specificity of 92% — substantially superior to FeNa (whose accuracy dropped significantly in the diuretic subgroup).
FEUrea Formula
FEUrea (%) = (UUrea × PCr) ÷ (PUrea × UCr) × 100
Prerenal example:
UUrea 400, PCr 2.4, PUrea 56, UCr 90
= (400 × 2.4) ÷ (56 × 90) × 100
= 960 ÷ 5,040 × 100
= 19.0% → Prerenal
FeNa Formula (Comparison)
FeNa (%) = (UNa × PCr) ÷ (PNa × UCr) × 100
Same patient (on furosemide):
UNa 65, PCr 2.4, PNa 140, UCr 90
= (65 × 2.4) ÷ (140 × 90) × 100
= 156 ÷ 12,600 × 100
= 1.24% → Falsely “indeterminate”
The key insight: In the example above, the same patient shows a FEUrea of 19% (clearly prerenal) but a FeNa of 1.24% (falsely indeterminate) because furosemide is inflating urinary sodium. This illustrates exactly why FEUrea is the preferred index in diuretic-treated patients — urea handling reflects the true tubular response to volume depletion, uncontaminated by the pharmacological effect of the diuretic.
Interpretation & Categories
FEUrea thresholds are well-established for differentiating prerenal from intrinsic AKI. The table below provides the standard classification alongside the corresponding FeNa values for comparison in patients who are not receiving diuretics.
| Category | FEUrea (%) | FeNa (%) — If No Diuretics | Interpretation |
|---|---|---|---|
| Prerenal | < 35% | < 1% | Intact tubular function — avid reabsorption of urea and sodium in response to hypoperfusion. Kidneys are functioning appropriately but underperfused. |
| Indeterminate | 35–50% | 1–2% | Grey zone — may represent early/evolving ATN, mixed prerenal and intrinsic pathology, or CKD with superimposed prerenal injury. Requires clinical correlation. |
| Intrinsic Renal | > 50% | > 2% | Tubular damage impairs passive urea reabsorption — urea is wasted in the urine. Most commonly seen in acute tubular necrosis (ATN). |
How Diuretics Affect Each Index
When FeNa and FEUrea disagree in a diuretic-treated patient, trust FEUrea. The most common discordant pattern is FEUrea <35% (prerenal) with FeNa >1% (falsely “intrinsic”) — this is the expected pharmacological effect of the diuretic, not a sign of tubular damage. If both indices point to intrinsic disease (FEUrea >50% and FeNa >2%), the diagnosis of ATN is strongly supported.
AKI Evaluation in the Diuretic-Treated Patient
Patients receiving diuretics who develop AKI present a particular diagnostic challenge. The very drugs designed to manage fluid overload can mask the renal indices that typically guide diagnosis. FEUrea is one of several tools that help navigate this challenge.
Patients with decompensated heart failure are among the most common clinical scenarios where FEUrea is essential. These patients often receive aggressive loop diuretic therapy to manage pulmonary oedema and peripheral congestion. However, over-diuresis can push them into prerenal AKI — a creatinine rise that is entirely reversible with volume repletion or diuretic dose reduction.
In this setting, FeNa is almost always elevated due to the diuretic effect and cannot reliably differentiate between “too much diuretic” (prerenal) and “true kidney injury” (cardiorenal syndrome / ATN). FEUrea <35% supports a prerenal mechanism and suggests that reducing the diuretic dose or providing cautious volume may improve renal function. FEUrea >50% suggests that tubular injury has occurred and a different management strategy is needed.
Serial FEUrea monitoring in heart failure can also track the trajectory — a rising FEUrea may indicate evolving tubular damage despite ongoing prerenal physiology, prompting earlier nephrology consultation.
Patients with cirrhosis and ascites are frequently treated with spironolactone and furosemide. When AKI develops, distinguishing hepatorenal syndrome (HRS) from ATN or prerenal AKI is critical — each requires a fundamentally different management approach. HRS is characterised by intense renal vasoconstriction with preserved tubular function, producing low FeNa (<1%) and low FEUrea (<35%).
However, the concurrent diuretic use confounds FeNa interpretation. FEUrea remains valuable in this setting: a FEUrea <35% supports either prerenal AKI or HRS (both involve preserved tubular function), while FEUrea >50% suggests ATN. The distinction between prerenal and HRS requires a diuretic withdrawal and albumin challenge — if creatinine does not improve after 48 hours of diuretic withdrawal and volume expansion with albumin (1 g/kg/day for 2 days), HRS should be considered.
ICU patients with sepsis-associated AKI frequently receive diuretics for fluid management, and many are oliguric despite apparently adequate resuscitation. The pathophysiology of sepsis-associated AKI is complex — it involves microvascular dysfunction, tubular inflammation, and altered haemodynamics that may not fit neatly into the prerenal/intrinsic dichotomy.
FEUrea can help in this context by identifying patients whose tubular function is preserved (FEUrea <35%), suggesting that optimising haemodynamics and perfusion may improve renal function. A FEUrea >50% suggests established tubular injury (ATN), which may take days to weeks to resolve. In practice, serial FEUrea measurements are more informative than single values in the ICU, as they track the trajectory of renal recovery or deterioration.
Novel biomarkers such as NGAL (neutrophil gelatinase-associated lipocalin) and KIM-1 (kidney injury molecule-1) may complement FEUrea in the ICU setting, providing earlier detection of tubular injury than traditional indices.
The landmark study by Carvounis et al. (2002) directly compared FeNa and FEUrea in 102 patients with AKI. In patients not on diuretics, both indices performed similarly — FeNa had a sensitivity of 90% and specificity of 82%, while FEUrea had a sensitivity of 90% and specificity of 96%. The real difference emerged in the diuretic subgroup: FeNa’s accuracy dropped substantially (many prerenal patients were misclassified), while FEUrea maintained its diagnostic performance.
Subsequent studies have confirmed that FEUrea is superior to FeNa in diuretic-treated patients. A meta-analysis by Diskin et al. found that FEUrea <35% had a pooled sensitivity of 79% and specificity of 89% for prerenal AKI across heterogeneous populations. The evidence supports using FEUrea as the first-line fractional excretion index whenever diuretics have been administered — and it is a reasonable adjunct even in patients not on diuretics.
Step 1: Determine if the patient has received diuretics within the past 24 hours. Step 2: If yes, prioritise FEUrea over FeNa. Step 3: Combine FEUrea with urine microscopy — muddy brown casts suggest ATN regardless of the index value. Step 4: If FEUrea is indeterminate (35–50%), consider a cautious fluid challenge and reassess within 24–48 hours.
Special Populations & Considerations
Clinical takeaway: FEUrea is most reliable in patients with previously normal renal function who develop AKI while receiving loop or thiazide diuretics. In CKD, extreme dietary protein variation, or neonates, interpret the result in the context of baseline values and trending measurements rather than relying on a single absolute threshold.
Common Pitfalls & Limitations
While FEUrea is unaffected by loop and thiazide diuretics, it can be influenced by osmotic diuresis. Mannitol infusion or severe hyperglycaemia (particularly in hyperosmolar hyperglycaemic state) generates an osmotic gradient in the proximal tubule that opposes passive urea reabsorption. This means FEUrea may be artificially elevated in these settings, potentially mimicking intrinsic renal disease when the kidneys are actually responding to a prerenal stimulus.
In patients with uncontrolled diabetes or those receiving mannitol (e.g., for raised intracranial pressure), interpret an elevated FEUrea with caution. Clinical context, urine sediment, and the response to correcting the underlying osmotic load are more reliable guides to diagnosis.
FEUrea is superior to FeNa specifically in the setting of diuretic use. In patients who are not receiving diuretics, FeNa has a slightly larger evidence base and is the more established index. Some studies have shown comparable or slightly better performance of FeNa over FEUrea in non-diuretic patients. The most robust approach is to calculate both indices when possible and interpret them together.
Additionally, FEUrea shares the same fundamental limitation as FeNa — it assesses tubular function, not the aetiology of injury. Intrinsic renal diseases that preserve tubular function early in their course (glomerulonephritis, contrast nephropathy, rhabdomyolysis) may show a low FEUrea despite active kidney injury. Always combine FEUrea with urine microscopy, imaging, and the clinical narrative.
The FEUrea formula assumes a relatively stable urea generation rate. In practice, several conditions alter urea production independently of kidney function. Upper GI bleeding increases urea production (absorbed blood protein is metabolised to urea in the liver), raising plasma urea and potentially lowering FEUrea — this may falsely suggest prerenal physiology even when ATN is present.
Conversely, severe liver disease reduces hepatic urea synthesis, lowering plasma urea and potentially raising FEUrea. In patients with fulminant hepatic failure, the BUN may be disproportionately low relative to creatinine, and FEUrea may overestimate the degree of tubular injury. Corticosteroid therapy also increases urea generation through enhanced protein catabolism, which may lower FEUrea independently of tubular function.
AKI is a dynamic process. A single FEUrea measurement provides a snapshot, but the clinical trajectory is often more informative than any one value. A patient with a FEUrea of 30% (prerenal) today may evolve to 55% (intrinsic) over the next 48 hours if ischaemic injury progresses to established ATN. Conversely, a falling FEUrea over serial measurements may indicate recovery of tubular function and a favourable prognosis.
In ICU patients, consider obtaining FEUrea at 12–24 hour intervals during evolving AKI. This allows you to detect the transition from prerenal to intrinsic disease — a window during which early intervention (optimising perfusion, withdrawing nephrotoxins) may still prevent established ATN.
Neither FEUrea nor FeNa can replace urine sediment examination. Muddy brown granular casts on microscopy are highly specific for ATN and may be present even when the FEUrea is in the indeterminate range (35–50%). Red cell casts point to glomerulonephritis, white cell casts suggest interstitial nephritis, and a bland sediment supports prerenal physiology.
The combination of FEUrea and urine microscopy is more powerful than either alone. In the landmark study by Perazella and colleagues, the urine microscopy score was independently associated with AKI severity and worsening — adding quantitative sediment analysis to fractional excretion indices significantly improved diagnostic accuracy. Always examine the sediment.
Quick Reference Summary
| Clinical Scenario | FEUrea | FeNa | Interpretation |
|---|---|---|---|
| Prerenal AKI, no diuretics | < 35% | < 1% | Concordant — strong prerenal evidence |
| Prerenal AKI, on diuretics | < 35% | 1–4% | Discordant — trust FEUrea (FeNa falsely elevated by diuretic) |
| ATN, no diuretics | > 50% | > 2% | Concordant — strong intrinsic evidence |
| ATN, on diuretics | > 50% | > 2% | Concordant — both elevated; ATN confirmed |
| GN / Contrast / Rhabdo (early) | Variable | < 1% | Low FeNa/FEUrea despite intrinsic disease — check sediment |
| CKD baseline | May be > 35% | May be > 1% | Baseline elevated — use trending, not absolute values |
If the patient is on diuretics, use FEUrea. FEUrea <35% = prerenal; FEUrea >50% = intrinsic. In the indeterminate zone (35–50%), combine with urine microscopy, clinical volume assessment, and a fluid challenge if appropriate. When FeNa and FEUrea disagree in a diuretic-treated patient, trust FEUrea. Neither index replaces looking at the urine under a microscope.
Disclaimer & References
For Educational Purposes Only. This calculator and the accompanying clinical information are intended as educational tools for healthcare professionals. They do not replace clinical judgement. Results should be interpreted in the full clinical context. Lab reference ranges vary by institution — verify with your own laboratory. Drug dosages should be confirmed against current prescribing information.
References
- 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;62(6):2223–2229. DOI: 10.1046/j.1523-1755.2002.00683.x
- Kaplan AA, Kohn OF. Fractional excretion of urea as a guide to renal dysfunction. American Journal of Nephrology. 1992;12(1–2):49–54. DOI: 10.1159/000168417
- Diskin CJ, Stokes TJ, Dansby LM, Radcliff L, Carter TB. The comparative benefits of the fractional excretion of urea and sodium in various azotemic oliguric states. Nephron Clinical Practice. 2010;114(2):c145–c150. DOI: 10.1159/000254387
- Espinel CH. The FeNa test: use in the differential diagnosis of acute renal failure. JAMA. 1976;236(6):579–581. DOI: 10.1001/jama.1976.03270060029022
- Perazella MA, Coca SG, Hall IE, Iber U, Parikh CR. Urine microscopy is associated with severity and worsening of acute kidney injury in hospitalized patients. Clinical Journal of the American Society of Nephrology. 2010;5(3):402–408. DOI: 10.2215/CJN.06960909
- Kellum JA, Lameire N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical Care. 2013;17(1):204. DOI: 10.1186/cc11454
- Bagshaw SM, Langenberg C, Wan L, May CN, Bellomo R. A systematic review of urinary findings in experimental septic acute renal failure. Critical Care Medicine. 2007;35(6):1592–1598. DOI: 10.1097/01.CCM.0000266684.17500.2F
- Steiner RW. Interpreting the fractional excretion of sodium. American Journal of Medicine. 1984;77(4):699–702. DOI: 10.1016/0002-9343(84)90368-1