In a 56‑year‑old man with massive melena‑induced hypotension and prerenal acute kidney injury, which adaptive response occurs: increased sodium excretion, reduced sodium excretion via tubuloglomerular feedback, promotion of diuresis, or promotion of natriuresis?

Adaptive Response to Prerenal AKI in Hemorrhagic Shock

In this patient with massive melena-induced hypovolemic shock and prerenal AKI, excretion of sodium is reduced via tubuloglomerular feedback and neurohormonal activation—this is the expected adaptive response to preserve intravascular volume and maintain renal perfusion.

Pathophysiology of Sodium Retention in Prerenal AKI

Primary Mechanism: Reduced Sodium Excretion

• Prerenal AKI from hemorrhagic shock triggers profound sodium retention as the kidney attempts to restore effective circulating volume 1
• Urine sodium concentration typically falls below 10 mEq/L in prerenal states, with fractional excretion of sodium (FENa) <1%, indicating avid sodium reabsorption 1, 2
• This patient's hypotension (BP 80/60) and volume depletion from melena activate compensatory mechanisms that prioritize sodium and water retention over excretion 1, 2

Neurohormonal Activation Drives Sodium Retention

• The renin-angiotensin-aldosterone system (RAAS) becomes markedly activated in response to reduced renal perfusion pressure, driving angiotensin II-mediated sodium reabsorption 1, 3
• Sympathetic nervous system (SNS) activation occurs simultaneously, further enhancing proximal tubular sodium reabsorption and reducing distal sodium delivery 1, 3
• Aldosterone secretion increases dramatically, promoting epithelial sodium channel (ENaC)-mediated sodium reabsorption in the collecting duct 1, 3

Tubuloglomerular Feedback Mechanism

• Reduced glomerular filtration from hypotension decreases sodium delivery to the distal tubule, triggering tubuloglomerular feedback that causes afferent arteriolar vasoconstriction 4
• This feedback mechanism further reduces GFR but preserves sodium by limiting filtered load 4
• The combined effect of reduced filtration and enhanced reabsorption results in minimal urinary sodium excretion 1, 2

Why the Other Options Are Incorrect

Steady Increase in Sodium Excretion (WRONG)

• This is physiologically opposite to what occurs in prerenal AKI—the kidney retains sodium, not excretes it 1, 2
• Increased sodium excretion would worsen hypovolemia and further compromise renal perfusion 1

Promotion of Diuresis (WRONG)

• Prerenal AKI typically presents with oliguria, not diuresis—urine output decreases as the kidney attempts to conserve volume 5, 6
• This patient's hypotension and volume depletion mandate water retention, not excretion 1
• Diuresis would be counterproductive and potentially fatal in hemorrhagic shock 2

Promotion of Natriuresis (WRONG)

• Natriuresis (sodium excretion) is the exact opposite of the adaptive response—the kidney aggressively retains sodium in prerenal states 1, 2
• FENa values in prerenal AKI are characteristically <1%, indicating sodium conservation, not excretion 1, 2

Clinical Implications and Management

Diagnostic Confirmation

• Urinary sodium <10 mEq/L and FENa <1% confirm prerenal etiology in this clinical context 1, 2
• Fractional excretion of urea (FEUrea) <28% may better discriminate prerenal AKI from acute tubular necrosis, especially if diuretics were recently used 1
• The urine:plasma creatinine ratio typically exceeds 20:1 in prerenal states 6

Therapeutic Approach

• Volume resuscitation with albumin (1 g/kg up to 100 g/day) is the cornerstone of treatment for hypovolemic prerenal AKI 1
• Red blood cell transfusion to maintain hemoglobin ≥8 g/dL is indicated given the significant melena 1
• All diuretics must be withdrawn immediately—they would worsen sodium depletion and renal perfusion 1
• Volume replacement should reduce serum creatinine to within 0.3 mg/dL of baseline if the AKI is purely prerenal 1

Critical Pitfall to Avoid

• Do not confuse prerenal AKI with acute tubular necrosis (ATN)—ATN presents with urine sodium >20 mEq/L, FENa >1%, and does not respond to volume resuscitation alone 1, 2
• Monitor for overtransfusion, which can cause volume overload and pulmonary edema, particularly in patients with underlying cardiac or liver disease 1