FEUrea Calculator (Fractional Excretion of Urea)

How to Use This Calculator

1. Enter urine urea, BUN (serum urea nitrogen), urine creatinine, and serum creatinine.
2. FEUrea% and interpretation display instantly.
3. FENa vs FEUrea tab: enter both sodium and urea values to compare both tests side-by-side.
4. Professional tier provides integrated AKI assessment from both markers.

Formula

Example

Frequently Asked Questions

• What is fractional excretion of urea (FEUrea)? ▼
  Fractional excretion of urea (FEUrea) measures the proportion of filtered urea that is excreted in the urine, using a formula analogous to FENa: FEUrea% = (Urine Urea × Serum Creatinine) / (Blood Urea Nitrogen × Urine Creatinine) × 100. Like FENa, it requires only a spot urine and paired serum samples. The physiological basis is that urea reabsorption in the kidney is largely passive, occurring in the collecting duct through urea transporters (UT-A1, UT-A3) driven by the corticomedullary osmotic gradient and ADH. In prerenal AKI, high ADH secretion and sodium-coupled water reabsorption concentrate the tubular fluid and increase passive urea reabsorption, resulting in a low FEUrea (<35%). In established ATN, the tubules are damaged and lose the capacity to concentrate urine and reabsorb urea normally, so more urea escapes into the final urine (FEUrea >50%). The key advantage over FENa is that urea reabsorption is not directly targeted by loop or thiazide diuretics, making FEUrea reliable in diuretic-treated patients. Carvounis et al. (Kidney Int 2002) validated FEUrea in 102 patients with AKI, including a subgroup on diuretics, demonstrating that FEUrea <35% identified prerenal AKI with 85% sensitivity and 92% specificity even when FENa was elevated due to diuretics.
• Why is FEUrea preferred over FENa in patients on diuretics? ▼
  Diuretics — particularly loop diuretics (furosemide, bumetanide, torsemide) and thiazides (hydrochlorothiazide, chlorthalidone) — directly block tubular sodium transporters (NKCC2 in the thick ascending limb and NCC in the distal tubule respectively). This pharmacological inhibition of sodium reabsorption increases urinary sodium excretion even in volume-depleted, prerenal states, falsely elevating FENa above the 1% threshold and misclassifying prerenal AKI as intrinsic ATN. This is a common clinical scenario: patients with chronic heart failure or cirrhosis who are on standing diuretic regimens may present with AKI from worsening decompensation (a prerenal mechanism) but have FENa >2% due to their diuretics, leading to incorrect diagnosis and management. Urea transporters in the collecting duct are not directly inhibited by loop or thiazide diuretics. While diuretics may have secondary effects on urinary concentrating ability (by reducing the medullary osmotic gradient), these effects are partial and do not abolish the FEUrea signal to the same degree. Acetazolamide (a carbonic anhydrase inhibitor) and mannitol (osmotic diuretic) can affect FEUrea, but these are less commonly used. The practical implication: when a patient on any diuretic presents with AKI, order FEUrea as the primary tubular function test. If neither diuretic use nor significant CKD is present, FENa and FEUrea are roughly equivalent.
• What FEUrea cutoff indicates prerenal AKI? ▼
  The widely accepted cutoff for prerenal AKI is FEUrea <35%, with values >50% suggesting intrinsic renal failure (typically ATN). The zone between 35% and 50% is considered indeterminate and requires clinical correlation. These thresholds were established in the Carvounis et al. 2002 study and have been validated in subsequent cohorts. It is important to understand that these cutoffs have diagnostic performance characteristics, not absolute rules: sensitivity ~85%, specificity ~92%, positive predictive value depending on pretest probability. A patient with septic AKI may have FEUrea <35% early in the course (when intrarenal vasoconstriction dominates and tubular function is partially preserved) but progress to ATN with FEUrea >50% within 24–48 hours. Serial measurement can track this transition. The diagnostic accuracy of FEUrea may be lower in non-oliguric AKI, where preserved urine flow is associated with less concentrating activity and intermediate urea reabsorption. Additionally, very high protein intake (enteral or parenteral nutrition) increases BUN disproportionately and may alter the FEUrea calculation. In contrast, liver failure reduces urea synthesis (low BUN) independent of renal function, potentially affecting interpretation — hepatorenal syndrome classically has both very low FENa and very low FEUrea, which is a useful pattern to recognize.
• Are there limitations to FEUrea accuracy? ▼
  Yes, FEUrea has several important limitations that clinicians must account for. First, high protein intake raises BUN and increases urea filtered load; the kidney must excrete more urea to maintain balance, which raises FEUrea even in prerenal states. Patients receiving high-protein enteral nutrition or total parenteral nutrition may have falsely elevated FEUrea. Second, severe hepatic failure significantly reduces urea synthesis — patients with cirrhosis or fulminant hepatic failure may have disproportionately low BUN relative to their degree of AKI, causing FEUrea to appear artificially low regardless of renal pathology. Third, high-dose corticosteroids increase protein catabolism and raise BUN, potentially altering the FEUrea calculation. Fourth, while FEUrea is less affected by loop and thiazide diuretics, it can still be affected by acetazolamide and osmotic agents. Fifth, FEUrea has been less extensively validated than FENa across different AKI populations, and most validation studies are small. Sixth, in contrast to FENa, most clinical laboratories do not routinely report urine urea — it must be specifically ordered, which may cause practical delays. Finally, as with all tubular function markers, FEUrea reflects a single moment in time. AKI evolves rapidly, and serial measurements are more informative than any single value. Always combine FEUrea with urine sediment examination (muddy brown casts = ATN, red cell casts = GN), clinical history, and urine osmolality.
• How accurate is FEUrea compared to FENa across different AKI types? ▼
  The relative diagnostic accuracy of FEUrea versus FENa depends primarily on whether diuretics are present. In diuretic-naive patients, both FENa and FEUrea have similar diagnostic accuracy for prerenal versus intrinsic AKI: sensitivity and specificity in the 85–95% range in the original validation studies, though these numbers are derived from relatively small cohorts (100–200 patients) with selected populations. Multiple subsequent studies confirm that in diuretic-naive patients with oliguric AKI, FENa performs at least as well as FEUrea, and some studies suggest FENa has marginally better specificity for prerenal AKI in this group. In patients on diuretics, FEUrea is clearly superior: Carvounis et al. demonstrated that FENa correctly classified only 48% of diuretic-treated patients, while FEUrea correctly classified 89%. In contrast nephropathy and myoglobinuria-related AKI, both FENa and FEUrea may be falsely low (< prerenal thresholds) despite established tubular injury — intrinsic ATN caused by hemoglobin or myoglobin toxicity is accompanied by intense renal vasoconstriction that maintains tubular sodium and urea avidity. These cases require clinical diagnosis (exposure history, CK levels, urinalysis for pigmented casts) rather than tubular function markers. In septic AKI — the most common form in the ICU — the pathophysiology is heterogeneous (microvascular, inflammatory, metabolic), and both FENa and FEUrea have reduced predictive value compared to hypovolemic AKI; they should be interpreted cautiously in this context.

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