Septic Shock Does NOT Cause Low FeNa
Septic shock is the answer that does NOT produce a low fractional excretion of sodium (FeNa). In fact, septic shock typically presents with a high FeNa due to acute tubular injury and impaired tubular sodium reabsorption, even in the early phases of sepsis 1.
Understanding FeNa in Different Shock States
Low FeNa (<1%) Conditions
The following conditions produce low FeNa through preserved tubular function and avid sodium reabsorption:
Hypovolemia from diarrhea: This represents classic prerenal azotemia where intact tubules avidly reabsorb sodium in response to volume depletion, producing FeNa <1% 2, 3
Low cardiac output states: Heart failure and cardiogenic shock cause renal hypoperfusion with neurohormonal activation (RAAS and SNS), leading to intense sodium retention and FeNa typically <1% 4, 2
Aminoglycoside administration: While aminoglycosides cause nephrotoxicity, they initially produce a prerenal pattern with low FeNa before progressing to tubular injury 5
High FeNa (>1%) in Septic Shock
Septic shock fundamentally differs from other shock states because it causes direct tubular injury even in early phases 1:
In sepsis patients, 77.3% had FeNa <1% and 63.2% had FEUrea <35% initially, but those with higher fractional sodium excretion had significantly elevated urinary NGAL (a marker of tubular injury) 1
Patients with FeNa >0.36% and FEUrea >31.5% had a 92% and 94.5% negative predictive value respectively for intrinsic AKI rather than transient prerenal injury 1
The combination of high FeNa and high FEUrea strongly predicts intrinsic (not prerenal) AKI in sepsis 1
Critical Pathophysiologic Distinction
The key difference is that septic shock causes:
- Direct tubular injury from inflammatory mediators, endotoxins, and microvascular dysfunction 1
- Impaired tubular sodium reabsorption despite systemic hypoperfusion 1
- Distributive shock physiology with high cardiac output and low systemic vascular resistance in early phases, unlike the low cardiac output seen in cardiogenic shock 6
In contrast, hypovolemia, low cardiac output, and early aminoglycoside exposure all preserve tubular integrity initially, allowing avid sodium reabsorption and low FeNa 2, 3.
Important Clinical Caveats
Do not assume low FeNa always means volume-responsive prerenal azotemia 3:
- Low FeNa can occur in acute glomerulonephritis, contrast nephrotoxicity, pigment nephropathy, and early acute tubular necrosis 3, 7
- Timing matters: FeNa measured very early in ARF (within 1-2 days) may still be low before converting to high values 7
- In established ARF, a low FeNa suggests superimposed volume depletion requiring fluid resuscitation 8
The clinical context determines interpretation 2, 3: A patient in septic shock with oliguria and elevated creatinine is far more likely to have intrinsic tubular injury (high FeNa) than prerenal azotemia, whereas the same FeNa value in a patient with diarrhea indicates volume depletion requiring aggressive fluid resuscitation 4, 1.