Fractional Excretion of Sodium (FeNa) Calculator
Differentiate prerenal from intrinsic renal causes of acute kidney injury using the fractional excretion of sodium. Also calculates FEUrea for patients on diuretics, where FeNa may be unreliable.
Calculate FeNa & FEUrea
Enter serum and urine sodium and creatinine values to calculate FeNa. To also calculate FEUrea (useful if the patient is on diuretics), enter serum and urine urea in the optional section below.
FeNa is a screening tool to help differentiate prerenal from intrinsic renal causes of AKI. It should always be interpreted alongside the full clinical picture — history, volume status, urine microscopy, and imaging. FeNa may be unreliable in patients receiving diuretics; use FEUrea in these cases.
Understanding Fractional Excretion of Sodium
The fractional excretion of sodium (FeNa) quantifies the percentage of filtered sodium that is ultimately excreted in the urine. In a healthy kidney responding to hypoperfusion, the tubules avidly reabsorb sodium, resulting in a very low FeNa (<1%). When the tubules are damaged (as in acute tubular necrosis), they lose their ability to reabsorb sodium efficiently, and the FeNa rises above 2%.
First described by Espinel in 1976, the FeNa rapidly became one of the most widely used bedside indices in nephrology. It leverages the fact that creatinine is freely filtered and not significantly reabsorbed — comparing sodium clearance to creatinine clearance effectively normalises sodium excretion for the glomerular filtration rate.
FeNa Formula
FeNa (%) = (UNa × PCr) ÷ (PNa × UCr) × 100
Example: UNa 12, PCr 2.0, PNa 140, UCr 120
= (12 × 2.0) ÷ (140 × 120) × 100
= 24 ÷ 16,800 × 100
= 0.14% → Prerenal
FEUrea Formula
FEUrea (%) = (UUrea × PCr) ÷ (PUrea × UCr) × 100
Example: UUrea 600, PCr 2.0, PUrea 40, UCr 120
= (600 × 2.0) ÷ (40 × 120) × 100
= 1,200 ÷ 4,800 × 100
= 25% → Prerenal (FEUrea <35%)
Key distinction: FeNa reflects tubular sodium handling, which is heavily influenced by diuretics. FEUrea reflects tubular urea handling, which is largely unaffected by loop and thiazide diuretics. In patients receiving diuretics, FEUrea <35% suggests prerenal physiology, while FEUrea >50% suggests intrinsic renal disease.
Interpretation & Categories
The FeNa value should be interpreted in the context of the patient’s clinical presentation, medication history, and underlying renal function. The table below summarises the standard interpretation thresholds for FeNa and FEUrea.
FeNa Classification
| FeNa (%) | Category | Interpretation | Typical Causes |
|---|---|---|---|
| < 1% | Prerenal | Intact tubular function — kidneys are avidly reabsorbing sodium in response to reduced perfusion | Hypovolaemia, heart failure, hepatorenal syndrome, renal artery stenosis |
| 1–2% | Indeterminate | May be seen in either prerenal or intrinsic disease — clinical correlation is essential | Early ATN, partial prerenal states, CKD with superimposed prerenal injury |
| > 2% | Intrinsic Renal | Tubular damage impairs sodium reabsorption — sodium is wasted in the urine | Acute tubular necrosis (ATN), acute interstitial nephritis, glomerulonephritis |
FEUrea Classification (For Patients on Diuretics)
A FeNa <1% does not always mean prerenal. Several intrinsic renal diseases preserve tubular sodium reabsorption early in their course — notably contrast nephropathy, myoglobinuric AKI (rhabdomyolysis), early obstructive uropathy, and acute glomerulonephritis. In these conditions, the FeNa may be <1% despite intrinsic renal damage. Always correlate with urine sediment analysis and clinical history.
Prerenal vs Intrinsic Renal Disease
The FeNa is one tool within a broader diagnostic framework for evaluating AKI. Differentiating prerenal from intrinsic causes is clinically critical because prerenal AKI is typically reversible with volume resuscitation, while intrinsic renal disease may require specific therapy and carries a different prognosis.
Prerenal AKI results from reduced renal perfusion with intact tubular function. The kidneys respond appropriately by conserving sodium and water. Common causes include hypovolaemia (haemorrhage, dehydration, GI losses), reduced cardiac output (heart failure, cardiogenic shock), systemic vasodilation (sepsis, cirrhosis), and renal vasoconstriction (NSAIDs, ACE inhibitors, hepatorenal syndrome).
Laboratory features supporting a prerenal diagnosis include FeNa <1%, urine sodium <20 mEq/L, urine osmolality >500 mOsm/kg, BUN:creatinine ratio >20:1, and a bland urine sediment (hyaline casts only, no muddy brown casts). The hallmark of prerenal AKI is its reversibility — serum creatinine should improve within 24–72 hours of adequate volume restoration.
ATN is the most common cause of intrinsic AKI. It results from ischaemic or nephrotoxic injury to the renal tubular epithelial cells. Ischaemic ATN typically follows prolonged prerenal states (severe hypotension, major surgery, septic shock), while nephrotoxic ATN is caused by agents such as aminoglycosides, cisplatin, radiocontrast, and endogenous toxins (myoglobin in rhabdomyolysis, haemoglobin in haemolysis).
Laboratory features include FeNa >2%, urine sodium >40 mEq/L, urine osmolality <350 mOsm/kg (isosthenuric — the tubules have lost concentrating ability), and characteristic muddy brown granular casts and renal tubular epithelial cells on urine microscopy. BUN:creatinine ratio is typically <20:1. Recovery usually occurs over 1–3 weeks as tubular cells regenerate.
Glomerulonephritis (GN): Acute GN can present with a FeNa <1% because the primary injury is at the glomerulus, not the tubules — tubular function may be initially preserved. Classic features include an active urine sediment (dysmorphic red blood cells, red cell casts), proteinuria, hypertension, and oedema. Serological workup (ANA, ANCA, anti-GBM, complement levels, ASO titres) is essential for aetiological diagnosis.
Acute Interstitial Nephritis (AIN): Most commonly drug-induced (antibiotics, NSAIDs, proton pump inhibitors), AIN presents with AKI, eosinophiluria (in some but not all cases), white cell casts, and sometimes a classic triad of fever, rash, and eosinophilia. The FeNa may be variable — often >1% but not universally >2%. Urine eosinophils have limited sensitivity and specificity; renal biopsy remains the gold standard for diagnosis when clinical suspicion is high.
Several important intrinsic renal conditions produce a FeNa <1%, potentially mimicking prerenal physiology and leading to diagnostic error. These include:
- Contrast-induced nephropathy: Renal vasoconstriction from contrast media reduces perfusion, and the initial tubular response is sodium avidity — FeNa may be <1% in the first 24–48 hours.
- Rhabdomyolysis: Myoglobin-induced tubular injury often presents early with FeNa <1% because myoglobin causes both vasoconstriction and direct tubular toxicity. Markedly elevated CK and dark urine are diagnostic clues.
- Acute glomerulonephritis: As above, glomerular injury with preserved tubular function yields low FeNa. Active urine sediment is the key distinguishing feature.
- Early obstructive uropathy: Bilateral ureteric obstruction or bladder outlet obstruction may initially present with low FeNa. Renal ultrasound is essential in the workup of any unexplained AKI.
- Atheroembolic disease: Cholesterol crystal embolisation to the renal vasculature can cause AKI with low FeNa due to renal vasoconstriction. Look for livedo reticularis, eosinophilia, and hypocomplementaemia.
FeNa is unreliable in patients on diuretics. Loop and thiazide diuretics block tubular sodium reabsorption, artificially raising the FeNa above 1% even in truly prerenal states. In diuretic-treated patients, use FEUrea (threshold <35% for prerenal) or interpret the FeNa with caution. Ideally, obtain samples before administering diuretics.
Special Populations & Considerations
Clinical takeaway: FeNa is most reliable when applied to oliguric patients with a rising creatinine who are not receiving diuretics, IV saline, or bicarbonate infusions. In all other scenarios, interpret with caution and consider FEUrea or other adjunctive tests (urine microscopy, renal ultrasound, biomarkers such as NGAL or KIM-1).
Common Pitfalls & Limitations
This is the single most common error. Diuretics directly block tubular sodium reabsorption, which inflates urinary sodium and therefore the FeNa — a patient with genuinely prerenal AKI may show a FeNa of 2–4% after receiving furosemide. If diuretics have been given, switch to FEUrea. Urea reabsorption in the proximal tubule is largely coupled to water reabsorption and is not significantly affected by loop diuretics, making FEUrea a more reliable index in this setting.
Ideally, collect urine for FeNa analysis before any diuretic is administered. In practice this is often not possible — document diuretic timing and use FEUrea alongside FeNa for a more complete assessment.
A FeNa <1% is often reflexively interpreted as prerenal, but several intrinsic renal diseases can present with a low FeNa. Contrast nephropathy, rhabdomyolysis-associated AKI, acute glomerulonephritis, early obstructive uropathy, and acute interstitial nephritis may all show FeNa <1% in their early phases. The key is to combine FeNa with urine sediment examination, imaging, and the clinical story.
A practical tip: if the clinical picture does not improve with appropriate volume resuscitation and the FeNa remains <1%, consider these alternative diagnoses rather than assuming the patient is still volume-depleted.
The original validation of FeNa was performed in oliguric patients. In non-oliguric AKI — which accounts for a large proportion of hospital-acquired AKI — the FeNa may be less discriminating. Non-oliguric ATN, for example, may present with a FeNa that overlaps with the prerenal range because some tubular function is preserved. Similarly, high-output renal failure can dilute urinary sodium, lowering the FeNa despite intrinsic damage.
In non-oliguric patients, urine microscopy and clinical response to a fluid challenge are often more informative than the FeNa alone.
Large-volume administration of normal saline (0.9% NaCl) delivers a significant sodium load, which increases urinary sodium excretion and may falsely elevate the FeNa. This is particularly relevant in emergency departments and ICUs where patients often receive several litres of crystalloid before urine studies are obtained.
Conversely, patients who are severely salt-restricted (low-sodium diets, adrenal insufficiency) may have very low urinary sodium regardless of renal tubular function. The timing of urine collection relative to IV fluid administration and dietary sodium intake should be considered when interpreting FeNa results.
The FeNa is a chemical test — it tells you about tubular sodium handling but nothing about the type of renal injury. Urine microscopy remains an indispensable tool in AKI evaluation. Muddy brown granular casts are highly specific for ATN. Red cell casts indicate glomerulonephritis. White cell casts suggest interstitial nephritis or pyelonephritis. A bland sediment with hyaline casts supports a prerenal diagnosis.
Over-reliance on FeNa at the expense of urine microscopy is a common error. The two tests are complementary — FeNa tells you “how much sodium?” and the sediment tells you “what is happening to the kidney?” Both are needed for a complete assessment.
Quick Reference Summary
| Parameter | Prerenal | Intrinsic (ATN) |
|---|---|---|
| FeNa | < 1% | > 2% |
| FEUrea | < 35% | > 50% |
| Urine Na⁺ | < 20 mEq/L | > 40 mEq/L |
| Urine osmolality | > 500 mOsm/kg | < 350 mOsm/kg |
| BUN : Creatinine ratio | > 20 : 1 | < 20 : 1 |
| Urine sediment | Bland / hyaline casts | Muddy brown granular casts, RTE cells |
| Response to fluids | Improves within 24–72 h | Does not improve |
FeNa is a screening tool — not a diagnosis. It is most useful as one data point among many. Always combine FeNa with urine microscopy, clinical volume assessment, medication history (especially diuretics), and imaging. When on diuretics, trust FEUrea over FeNa. A low FeNa does not always mean prerenal — consider contrast nephropathy, rhabdomyolysis, GN, and early obstruction.
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
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- Diskin CJ, Stokes TJ, Dansby LM, Radcliff L, Carter TB. Towards an understanding of overt nephrogenic diabetes insipidus: the fractional excretion of urea and electrolyte-free water. Clinical Nephrology. 2008;69(1):48–52. DOI: 10.5414/CNP69048
- 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
- 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
- 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
- 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