Printed on 3/17/2026
For informational purposes only. This is not medical advice.
The Fractional Excretion of Sodium (FENa) is a laboratory calculation used to differentiate pre-renal azotemia (FENa <1%) from intrinsic renal disease (FENa >2%) in patients with acute kidney injury (AKI). It measures the percentage of filtered sodium that is excreted in the urine. In pre-renal states (dehydration, heart failure), the kidneys avidly reabsorb sodium, yielding a low FENa. In intrinsic renal disease (ATN), tubular damage impairs sodium reabsorption, yielding a high FENa. The test requires simultaneous urine and serum sodium and creatinine measurements. Use alongside [BUN/Creatinine Ratio](/tools/bun-creatinine-ratio) and track baseline kidney function with [eGFR Calculator](/tools/egfr-calculator). In cirrhotic patients, also assess disease severity with [MELD Score](/tools/meld-score).
Formula: FENa (%) = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100
Obtain a spot urine sample (no need for 24-hour collection) and draw serum labs at the same time. The urine sample should be sent for sodium and creatinine. The serum sample (from a basic metabolic panel) provides sodium and creatinine. Timing is critical: ideally collect before starting IV fluids, diuretics, or other interventions that could alter sodium handling. If the patient is on diuretics, FENa will be unreliable — consider FEUrea instead. Document the timing of sample collection relative to any fluid boluses or medications.
The FENa formula is: FENa (%) = [(Urine Na × Serum Cr) / (Serum Na × Urine Cr)] × 100. This represents the percentage of filtered sodium that is excreted in the urine rather than reabsorbed by the tubules. For example, if urine Na = 15 mEq/L, serum Na = 140 mEq/L, urine Cr = 100 mg/dL, and serum Cr = 2.0 mg/dL: FENa = [(15 × 2.0) / (140 × 100)] × 100 = 0.21%. This low value suggests pre-renal azotemia. Normal kidneys can reabsorb >99% of filtered sodium, so even a FENa of 1% indicates impaired tubular function.
FENa <1% suggests pre-renal azotemia (dehydration, heart failure, hepatorenal syndrome) — the kidneys are intact and appropriately conserving sodium. FENa >2% suggests intrinsic renal disease, most commonly acute tubular necrosis (ATN) — the damaged tubules cannot reabsorb sodium. FENa 1–2% is indeterminate and requires additional clinical information. Always correlate with urine sediment (muddy brown casts suggest ATN, hyaline casts suggest pre-renal), clinical exam (volume status), and response to fluid challenge. If pre-renal, creatinine should improve with fluid resuscitation. If ATN, creatinine will remain elevated despite volume repletion.
Hospitalists, nephrologists, intensivists
FENa is the first-line test to differentiate pre-renal azotemia from intrinsic renal injury when a patient develops rising creatinine. A low FENa (<1%) indicates pre-renal physiology — treat with volume resuscitation. A high FENa (>2%) suggests ATN or other intrinsic disease — supportive care, avoid nephrotoxins, and consider nephrology consultation. This distinction guides immediate management and prevents unnecessary interventions (e.g., avoiding aggressive fluid loading in established ATN).
Emergency physicians, ED nurses
When a patient presents with oliguria and elevated creatinine, FENa helps determine whether this is reversible pre-renal AKI (requiring IV fluids) or established intrinsic renal failure (where excessive fluids could cause volume overload). Send spot urine sodium and creatinine along with serum labs, calculate FENa, and use the result to guide disposition and fluid management. Pre-renal patients may be discharged after fluid resuscitation; intrinsic AKI often requires admission and nephrology consult.
Cardiologists, nephrologists
In heart failure patients with worsening renal function on diuretics, FENa helps determine whether kidney dysfunction is truly worsening (high FENa, intrinsic damage from hypoperfusion or nephrotoxins) or whether the kidneys are appropriately responding to decreased perfusion (low FENa, suggesting need for hemodynamic optimization rather than stopping diuretics). Note: FENa is unreliable while actively on diuretics — use FEUrea, or hold diuretics 24–48 hours before testing if safe.
Hepatologists, gastroenterologists, ICU physicians
Hepatorenal syndrome (HRS) presents with AKI in cirrhotic patients with very low FENa (<1%), low urine sodium (<10 mEq/L), and no response to volume challenge. FENa helps distinguish HRS from ATN (which would have FENa >2%). This distinction is critical because HRS may respond to vasoconstrictor therapy (midodrine, octreotide, or terlipressin) and albumin, while ATN requires supportive care and consideration of renal replacement therapy. HRS diagnosis requires FENa <1% as one of the diagnostic criteria.
Trauma surgeons, emergency medicine, nephrologists
Rhabdomyolysis can cause AKI via myoglobin-induced tubular injury. Interestingly, myoglobinuric AKI often presents with low FENa (<1%) despite being intrinsic renal disease, because myoglobin injury is initially intratubular and doesn't immediately damage sodium reabsorption. This is a known exception where FENa can be misleadingly low. Look for elevated CK (>5,000–10,000), tea-colored urine, and positive urine myoglobin. Treatment is aggressive IV fluid hydration (goal urine output 200–300 mL/hr) to flush myoglobin.
Nephrologists, medical students, residents
FENa is a foundational concept in renal physiology education. It teaches tubular sodium handling, the difference between glomerular filtration and tubular reabsorption, and clinical reasoning in AKI. Understanding FENa's limitations (diuretics, CKD, exceptions) develops sophisticated clinical thinking. It's commonly included in nephrology board exams and is a standard bedside teaching tool during nephrology rounds. Calculating FENa reinforces the pathophysiology of pre-renal vs intrinsic AKI.
Diuretics (furosemide, HCTZ, etc.) increase urinary sodium excretion, causing FENa to be artificially elevated even in pre-renal states. A patient with true pre-renal azotemia on diuretics may have FENa >2%, falsely suggesting intrinsic renal disease. In diuretic-treated patients, use Fractional Excretion of Urea (FEUrea) instead — urea handling is less affected by diuretics. FEUrea <35% suggests pre-renal; >50% suggests intrinsic. Always ask about diuretic use before ordering FENa.
FENa is most accurate when measured early in the course of AKI, before therapeutic interventions. Once you give IV fluids, the kidneys' sodium handling may change. Ideally, send the spot urine sample and draw serum labs at the time of AKI recognition, before the first liter of saline. Document the timing. If you must give urgent fluids (hypotensive patient), get the samples as soon as possible, but note that results may be less reliable.
FENa between 1% and 2% is indeterminate and doesn't clearly favor pre-renal or intrinsic disease. In this range, look at urine sediment (muddy brown casts = ATN), clinical volume status (dry mucous membranes, flat JVP = pre-renal), [BUN/Creatinine Ratio](/tools/bun-creatinine-ratio) (>20 favors pre-renal), and response to fluid challenge. If creatinine improves after 1–2 liters of IV fluid, it was pre-renal. If no improvement, it's likely intrinsic. Track kidney function with [eGFR Calculator](/tools/egfr-calculator).
Certain intrinsic renal diseases can present with FENa <1%, mimicking pre-renal physiology: (1) Contrast-induced nephropathy, (2) Myoglobinuric AKI (rhabdomyolysis), (3) Early ATN (before tubular damage is complete), (4) Acute glomerulonephritis, (5) Acute interstitial nephritis (sometimes). Don't assume FENa <1% always means pre-renal — consider the clinical context and other diagnostic clues.
If you can't calculate FENa (missing values), urine sodium alone provides useful information: Urine Na <20 mEq/L suggests pre-renal azotemia (kidneys conserving sodium). Urine Na >40 mEq/L suggests intrinsic renal disease (kidneys wasting sodium). This is less precise than FENa but still clinically helpful. Some clinicians prefer urine sodium for its simplicity, especially in resource-limited settings.
Patients with CKD have adapted tubular function — their remaining nephrons excrete more sodium per nephron to maintain balance. This means CKD patients may have higher baseline FENa (1–2%) even when euvolemic. When CKD patients develop AKI, FENa interpretation becomes tricky. Focus more on change from baseline, clinical volume assessment, and comparison to prior values if available.
Write: 'FENa 0.4% consistent with pre-renal azotemia. Patient dry on exam (dry mucous membranes, flat JVP). BUN/Cr 28:1.4 = 20 (supports pre-renal). Urine sediment: hyaline casts, no cells. Plan: 2L NS bolus, recheck creatinine in 6 hours.' This documentation shows systematic thinking and provides a clear plan. If creatinine doesn't improve despite fluids, you've established that it's not purely pre-renal.
FENa is a screening tool, but the gold standard for diagnosing pre-renal azotemia is creatinine improvement after volume resuscitation. Give 1–2 liters of IV normal saline (if not volume overloaded) and recheck creatinine in 6–12 hours. If creatinine drops significantly, it was pre-renal. If no change or worsening, it's intrinsic or post-renal. Therapeutic response confirms diagnosis.
Fractional Excretion of Urea (FEUrea) uses the same formula structure but replaces sodium with urea. FEUrea <35% suggests pre-renal; >50% suggests intrinsic. It's more reliable than FENa in patients on diuretics or with glycosuria. However, FEUrea requires a urine urea nitrogen measurement, which is not routinely available in all labs. Order it specifically when FENa is unreliable.
FENa tells you about tubular sodium handling, but urinalysis reveals the type of kidney injury: Muddy brown casts = ATN. RBC casts = glomerulonephritis. WBC casts = interstitial nephritis. Hyaline casts only = pre-renal or non-specific. Eosinophiluria = allergic interstitial nephritis. The combination of FENa + urinalysis + clinical exam gives you the complete picture. Order both tests together in any AKI workup.
Your FENa result helps classify the etiology of acute kidney injury (AKI). A FENa below 1% suggests pre-renal azotemia — the kidneys are intact and appropriately conserving sodium in response to decreased renal perfusion. Common causes include dehydration, hemorrhage, heart failure, and hepatorenal syndrome. The kidney tubules are functioning normally and avidly reabsorbing sodium and water to maintain intravascular volume.
A FENa between 1% and 2% falls in an indeterminate zone that may represent either pre-renal or intrinsic renal disease, and additional clinical context is needed. A FENa above 2% suggests intrinsic renal disease, most commonly acute tubular necrosis (ATN), where damaged tubules can no longer effectively reabsorb sodium. Other causes include interstitial nephritis and acute glomerulonephritis. The FENa result should always be interpreted alongside the clinical presentation, urinalysis findings, and imaging.
Use FENa as part of the initial workup of acute kidney injury when you need to differentiate between pre-renal azotemia and intrinsic renal disease. It is most valuable in oliguric patients with a rising creatinine where the clinical distinction between volume depletion and tubular injury is uncertain. The test requires simultaneous measurement of urine sodium, serum sodium, urine creatinine, and serum creatinine — ideally obtained before any interventions.
FENa is most commonly calculated in the emergency department, inpatient wards, and ICU settings during the evaluation of new-onset AKI. It is a standard component of the nephrology consultation workup and is taught as a foundational concept in renal physiology and clinical medicine.
FENa is unreliable in patients receiving diuretics, which increase urinary sodium excretion and falsely elevate FENa even in pre-renal states. In diuretic-treated patients, the Fractional Excretion of Urea (FEUrea) is preferred because urea handling is less affected by diuretics. FENa is also unreliable in the setting of glycosuria (e.g., DKA), recent contrast dye administration, and chronic kidney disease where tubular adaptation has occurred.
Importantly, some causes of intrinsic renal disease can present with a low FENa (<1%), mimicking pre-renal physiology. These include contrast nephropathy, myoglobinuria (rhabdomyolysis), early ATN (before tubular damage is established), and acute glomerulonephritis. Conversely, pre-renal states superimposed on chronic kidney disease may show higher-than-expected FENa values. The test is most accurate when applied early in the course of AKI and before therapeutic interventions.
For related assessments, see eGFR Calculator and Creatinine Clearance.
Disclaimer: This tool is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about your health.
Calculate estimated glomerular filtration rate (eGFR) using the CKD-EPI 2021 race-free equation. Free kidney function assessment with CKD staging from serum creatinine.
ClinicalCalculate creatinine clearance (CrCl) using the Cockcroft-Gault equation. Used for renal drug dosing adjustments based on kidney function.