Fractional Excretion of Sodium (FeNa) in Acute Kidney Injury
Direct Interpretation
FeNa <1% suggests prerenal causes including volume depletion or hepatorenal syndrome, but has extremely poor specificity (only 14%) and cannot reliably exclude intrinsic kidney disease, particularly in cirrhosis. 1, 2
Understanding the Limitations
FeNa is fundamentally flawed as a standalone diagnostic test because:
- In cirrhosis patients: FeNa <1% has 100% sensitivity but only 14% specificity for prerenal causes, meaning most patients with intrinsic kidney disease can also have low FeNa 1, 2
- With diuretic use: FENa becomes unreliable as diuretics increase sodium excretion regardless of the underlying cause, artificially elevating FENa even in true prerenal states 3, 4
- In various intrinsic renal diseases: Low FeNa (<1%) can occur in acute glomerulonephritis, contrast nephropathy, pigment nephropathy, acute obstruction, and non-oliguric acute renal failure 3, 5
- In cardiac or hepatic failure: FeNa remains low despite these not being volume-responsive processes 3
Superior Alternative: Fractional Excretion of Urea (FEUrea)
Use FEUrea instead of FeNa, especially if diuretics have been administered within the past week. 4, 6
- FEUrea <35% indicates prerenal azotemia with 89% sensitivity in diuretic-treated patients versus only 48% for FENa <1% 4
- FEUrea <28% has 75% sensitivity and 83% specificity for hepatorenal syndrome versus other causes in cirrhosis 2
- FEUrea remains accurate in diuretic-treated patients because urea reabsorption depends on passive forces rather than active transport 4, 6
Clinical Management Algorithm
Stage 1: Immediate Actions (All AKI Patients)
- Withdraw all nephrotoxic medications immediately: NSAIDs, ACE inhibitors, ARBs, aminoglycosides, contrast agents 1, 2
- Hold or reduce diuretics and review all medications including over-the-counter drugs 1, 2
- Obtain urine studies before volume expansion: urinalysis with microscopy, urine sodium, calculate both FeNa and FEUrea 1, 2
Stage 2: Assess for Volume Depletion
Look specifically for:
- Recent diuretic escalation, vomiting, diarrhea, hemorrhage, or third-spacing 2
- In cirrhosis: spontaneous bacterial peritonitis (most common trigger for hepatorenal syndrome) 1
- Blood loss requiring transfusion to maintain hemoglobin ≥8 g/dL 1
Stage 3: Therapeutic Trial with Albumin
If clinical hypovolemia is suspected, administer albumin 1 g/kg/day (maximum 100 g/day) for 2 consecutive days. 1, 2
- Monitor carefully for volume overload and pulmonary edema 1, 2
- Response defined as: return of serum creatinine to within 0.3 mg/dL of baseline 1
- If no response after 48 hours, this is NOT simple prerenal azotemia 1
Stage 4: Interpretation Based on Response
Responders (creatinine improves to within 0.3 mg/dL of baseline):
- Diagnosis: Prerenal AKI (hypovolemic) 1
- Monitor creatinine every 2-4 days during hospitalization 2
- Outpatient follow-up every 2-4 weeks for 6 months 2
Non-responders with progression:
- Consider hepatorenal syndrome if cirrhosis present (check FEUrea <28%) 2
- Consider acute tubular necrosis if FEUrea >35% 4
- Examine urine sediment: muddy brown casts confirm ATN, RBC casts indicate glomerulonephritis requiring nephrology consultation 2
Critical Pitfalls to Avoid
- Never rely on FeNa alone without considering recent diuretic use, clinical context, and urine sediment 1, 3
- Do not use BUN:Cr ratio as it is heavily influenced by GI bleeding, protein intake, and catabolic states 2
- Do not calculate baseline creatinine using reverse MDRD formula in cirrhosis—it is inaccurate and adds bias 1, 2
- Recognize that low FeNa during ATN recovery may indicate superimposed volume depletion requiring additional fluid resuscitation 7
- In non-oliguric acute renal failure, both FeNa and FEUrea may be unreliable regardless of etiology 3, 5
Long-Term Implications
Even patients who fully recover from prerenal AKI remain at increased risk for recurrent AKI, chronic kidney disease progression, cardiovascular events, and mortality, mandating close long-term follow-up. 2