Calculate FENa to differentiate prerenal from intrinsic renal AKI. Includes FENa formula, AKI diagnostic indices comparison, and clinical interpretation with diuretic use guidance.
The Fractional Excretion of Sodium (FENa) Calculator computes the percentage of filtered sodium that is excreted in the urine, the most widely used urinary index for differentiating prerenal azotemia from intrinsic renal acute kidney injury (AKI). FENa reflects the kidney's ability to reabsorb sodium: in prerenal states (volume depletion, heart failure), the kidneys avidly reabsorb sodium, yielding a FENa < 1%. In intrinsic tubular damage (ATN), the damaged tubules cannot reabsorb sodium efficiently, resulting in FENa > 2%.
First described by Espinel (1976) and refined by Miller et al. (1978), FENa remains a cornerstone of the AKI workup. It requires four simultaneous measurements: urine sodium, plasma sodium, urine creatinine, and plasma creatinine. The formula normalizes sodium excretion to creatinine excretion, eliminating the need for timed urine collections.
Critical limitations include unreliability with diuretic use (diuretics increase sodium excretion, falsely elevating FENa) and several intrinsic renal conditions that paradoxically maintain low FENa (contrast nephropathy, rhabdomyolysis, acute glomerulonephritis). In diuretic-treated patients, FEUrea is the preferred alternative. The calculator includes unit conversions, clinical context assessment, and a comprehensive comparison table of AKI diagnostic indices.
FENa is one of the first tests ordered in the AKI workup, but its interpretation requires understanding its limitations. This calculator provides the numerical result plus clinical context — highlighting when FENa may be misleading (diuretics, CKD, specific diseases) and suggesting complementary studies. Keep these notes focused on your operational context.
FENa (%) = (UNa × PCr) / (PNa × UCr) × 100 Where: • UNa = Urine sodium (mEq/L) • PNa = Plasma sodium (mEq/L) • UCr = Urine creatinine (mg/dL) • PCr = Plasma creatinine (mg/dL) Interpretation: • FENa < 1%: Prerenal AKI • FENa 1–2%: Indeterminate • FENa > 2%: Intrinsic renal AKI (likely ATN)
Result: FENa = 0.12% — Prerenal AKI
FENa = (10 × 2.0) / (140 × 120) × 100 = 20/16800 × 100 = 0.12%. This very low FENa (<1%) indicates the kidneys are avidly reabsorbing sodium, consistent with prerenal azotemia (volume depletion, heart failure, etc.). The high urine creatinine relative to plasma creatinine (ratio 60) further supports intact tubular concentrating ability.
FENa is one component of a comprehensive AKI evaluation that includes: history/physical (volume status, medications, nephrotoxin exposure), urinalysis with microscopy, serum chemistries (BUN, creatinine, electrolytes), urine chemistries (Na, Cr, osmolality), renal ultrasound (obstruction, kidney size), and sometimes renal biopsy. No single test is diagnostic — the combination of findings guides classification into prerenal, intrinsic (glomerular, tubular, interstitial, vascular), or postrenal causes.
Traditional indices like FENa have significant limitations. Novel AKI biomarkers include NGAL (rises within 2 hours of injury, before creatinine), KIM-1 (specific for proximal tubular injury), IL-18 (inflammatory marker), and TIMP-2×IGFBP7 (NephroCheck, FDA-cleared for AKI risk prediction in ICU). These biomarkers detect tubular injury before functional decline (creatinine rise) and distinguish "prerenal AKI" that will progress to ATN from that which will resolve with volume repletion.
In practice, FENa should prompt action rather than be viewed as a definitive diagnosis. FENa <1% in a dehydrated patient → fluid resuscitation trial. FENa >2% with muddy brown casts → likely ATN, avoid further nephrotoxins, supportive care. FENa 1–2% → obtain additional data (FEUrea, urine microscopy, ultrasound). The most common mistake is over-reliance on a single FENa value without considering the full clinical picture.
FENa measures the percentage of sodium filtered by the glomeruli that ends up in the urine. Normally, the kidneys reabsorb >99% of filtered sodium (FENa ~1%). In prerenal states, the kidneys reabsorb even more sodium (FENa <1%) to conserve volume. When tubules are damaged (ATN), they lose the ability to efficiently reabsorb sodium, and FENa rises above 2%. By normalizing to creatinine (which is freely filtered and not reabsorbed), a spot urine sample can be used instead of a 24-hour collection.
Diuretics (especially loop diuretics like furosemide) directly block sodium reabsorption in the tubules, artificially increasing urine sodium and FENa. A prerenal patient on diuretics may have FENa >1%, leading to misclassification as intrinsic AKI. FEUrea (fractional excretion of urea) is less affected because urea reabsorption occurs primarily in the collecting duct, which is not the site of action of most diuretics. FEUrea <35% suggests prerenal even in diuretic-treated patients.
Several intrinsic renal conditions maintain FENa <1% early in their course: 1) Contrast nephropathy — intense vasoconstriction reduces sodium delivery; 2) Rhabdomyolysis — myoglobin causes vasoconstriction; 3) Acute glomerulonephritis — glomerular inflammation without primary tubular damage; 4) Early sepsis — hemodynamic changes precede tubular injury; 5) Acute urinary obstruction — back-pressure reduces filtration initially. These are important false negatives that require clinical correlation.
Complementary tests include: Urine microscopy (most specific: muddy brown granular casts = ATN, bland sediment = prerenal), urine osmolality (>500 prerenal, <350 ATN), BUN/Cr ratio (>20 prerenal, <15 ATN), FEUrea (<35% prerenal, >50% intrinsic), and urine specific gravity (>1.020 prerenal). Novel biomarkers (NGAL, KIM-1, IL-18) detect tubular injury before creatinine rises. A fluid challenge (250–500 mL bolus with creatinine monitoring) can also distinguish: improvement suggests prerenal.
In a healthy person on a normal sodium diet, FENa is approximately 0.5–1.5%. It varies with dietary sodium intake: low-sodium diet → FENa decreases (<0.5%), high-sodium diet → FENa increases (>1%). In the context of AKI, FENa <1% suggests prerenal and >2% suggests intrinsic. The 1–2% "gray zone" requires additional clinical information for interpretation. In neonates, normal FENa is higher (up to 5%) due to immature tubular function.
FENa has limited utility in CKD patients developing AKI ("acute-on-chronic"). In CKD, baseline FENa is already elevated (>1%) because remaining nephrons must increase per-nephron sodium excretion to maintain sodium balance. A "normal" FENa in CKD may actually represent prerenal physiology. Trending FENa over time (increasing vs stable) may be more useful than a single value. Clinical context, urine output trends, and volume assessment remain paramount in CKD patients with AKI.