FENa Calculator (Fractional Excretion of Sodium)

How to Use This Calculator

1. Enter urine sodium, serum sodium, urine creatinine, and serum creatinine.
2. FENa% and interpretation (prerenal/indeterminate/ATN) display instantly.
3. Limitations tab: flag diuretic use or CKD to see reliability assessment.
4. Professional tier adds FEUrea, BUN/Cr ratio, and urine osmolality context.

Formula

Example

Frequently Asked Questions

• What is fractional excretion of sodium (FENa)? ▼
  Fractional excretion of sodium (FENa) is the percentage of filtered sodium that is excreted in the urine. It is calculated from a single spot urine and paired serum sample using the formula: FENa% = (Urine Na × Serum Creatinine) / (Serum Na × Urine Creatinine) × 100. The logic is that creatinine excretion serves as a surrogate for GFR: by expressing sodium excretion as a fraction of creatinine excretion (which approximates filtered load), we normalize for differences in urine concentration and flow rate. FENa was introduced by Espinel in 1976 as a practical bedside test to differentiate prerenal acute kidney injury (AKI) from established intrinsic renal failure, most commonly acute tubular necrosis (ATN). In prerenal AKI, reduced renal perfusion triggers maximal tubular sodium reabsorption — the kidney conserves sodium to restore intravascular volume, resulting in FENa <1%. In ATN, tubular damage impairs the ability to reabsorb sodium, so a larger fraction escapes into the urine, typically producing FENa >2%. Values between 1% and 2% are indeterminate. FENa is most reliable in oliguric AKI (<400 mL/day urine output) in patients not taking diuretics and without pre-existing CKD.
• When is FENa <1% diagnostic for prerenal AKI? ▼
  FENa <1% is most reliable as a marker of prerenal AKI when: (1) The patient is oliguric — urine output <400 mL/24 hours. Non-oliguric AKI (preserved urine output) is often ATN, and FENa can be low or normal in this setting. (2) The patient is not on diuretics — particularly loop diuretics (furosemide, bumetanide) or thiazides, which directly increase urinary sodium excretion, falsely elevating FENa even in prerenal states. (3) There is no underlying CKD — chronic tubulointerstitial damage from CKD alters baseline sodium handling. (4) The clinical picture is consistent: volume depletion (bleeding, vomiting, diarrhea), cardiorenal syndrome, or hepatorenal syndrome. In these contexts, FENa <1% has a sensitivity of ~90% and specificity of ~90% for prerenal AKI in the original Espinel 1976 cohort. Important exceptions where FENa can be <1% despite intrinsic AKI: contrast nephropathy (early), myoglobinuria (rhabdomyolysis-associated ATN), hemoglobinuria, early obstructive uropathy, and acute glomerulonephritis. These conditions cause intense tubular vasoconstriction and sodium avidity despite ongoing intrinsic renal injury. Therefore, FENa should never be interpreted in isolation — it must be contextualized with clinical history, urine sediment, and trends in creatinine.
• Why does FENa fail in patients taking diuretics? ▼
  Loop diuretics (furosemide, bumetanide, torsemide) and thiazides inhibit tubular sodium transporters in the thick ascending limb of the Loop of Henle and distal convoluted tubule respectively, directly causing natriuresis regardless of the patient's volume status. A patient who is profoundly volume-depleted (prerenal AKI) but recently received furosemide will have high urinary sodium and an elevated FENa — often >2% — even though their kidneys are functionally intact and attempting sodium conservation when not inhibited by the drug. Studies show that furosemide can raise FENa from <1% to >3% within 4–6 hours of a single dose, and the effect can persist for 8–12 hours after the last dose. The same limitation applies to any condition that independently raises urinary sodium: syndrome of inappropriate antidiuretic hormone secretion (SIADH), adrenal insufficiency, salt-wasting nephropathy, and osmotic diuresis (glucosuria, mannitol). In patients on diuretics, fractional excretion of urea (FEUrea) is the preferred alternative because urea reabsorption occurs by passive mechanisms in the collecting duct and is less directly affected by loop/thiazide diuretics. FEUrea <35% suggests prerenal AKI with good sensitivity even in patients receiving diuretics. When diuretic use is documented, clinicians should either wait for the drug to wear off (if clinically feasible) or use FEUrea instead of FENa.
• When should FEUrea be used instead of FENa? ▼
  Fractional excretion of urea (FEUrea) should replace FENa as the primary tubular function test in any clinical scenario where sodium handling is pharmacologically or pathologically altered. The clearest indication is diuretic use: loop and thiazide diuretics block tubular sodium reabsorption, making FENa unreliable, while urea reabsorption is primarily passive and occurs in the collecting duct via urea transporters, driven by ADH-dependent mechanisms largely independent of sodium transporters. Carvounis et al. (Kidney Int 2002) demonstrated that FEUrea <35% identifies prerenal AKI with 85% sensitivity and 92% specificity in patients on diuretics, comparable to FENa performance in diuretic-naive patients. Other indications for FEUrea over FENa include: CKD with baseline sodium handling abnormalities, hepatorenal syndrome (where tubular sodium avidity is extreme and complicates interpretation), contrast-induced AKI (FENa often <1% regardless), and myoglobinuria/hemoglobinuria. Limitations of FEUrea: it also becomes less reliable in patients receiving urea-affecting medications, in severe hepatic failure (reduced urea production), and in high-protein intake states. When both FENa and FEUrea are available and concordant, diagnostic confidence is higher. When they are discordant (e.g., FENa >2% but FEUrea <35%), diuretic effect on FENa is the most likely explanation — FEUrea should be trusted in that context.
• Can FENa diagnose obstructive uropathy or hepatorenal syndrome? ▼
  FENa has limited and sometimes misleading diagnostic value in both obstructive uropathy and hepatorenal syndrome. In acute obstructive uropathy (obstruction present for <24 hours), FENa is typically <1% because tubular function is initially preserved and the kidney responds to backpressure by conserving sodium — a prerenal-like pattern. However, after prolonged obstruction (>48-72 hours), tubular injury develops and FENa may rise above 2%, mimicking ATN. Relief of the obstruction (catheterization, ureteral stent) is both diagnostic and therapeutic, and FENa does not help guide this decision. In hepatorenal syndrome (HRS), FENa is characteristically extremely low (<0.1%) because intense renal vasoconstriction and maximal neurohormonal activation (RAAS, sympathetic, ADH) drive near-total sodium reabsorption. An FENa <0.1% in a patient with cirrhosis and AKI strongly supports HRS over ATN, which is a clinically useful distinction. However, HRS is a diagnosis of exclusion — AKI in cirrhosis has many causes (infection, hypovolemia, nephrotoxins, GN) and FENa alone does not establish the diagnosis. The diagnosis requires exclusion of volume depletion, nephrotoxin withdrawal, infection control, and absence of response to volume expansion. FENa therefore serves as one supporting data point in this context, not a standalone diagnostic test.

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