A 65-year-old man with HFrEF (LVEF 25%) presents with serum sodium 128 mEq/L, serum creatinine 1.8 mg/dL (baseline 1.2 mg/dL), and worsening renal function despite diuretic therapy. BNP is 2800 pg/mL. Which mechanism best explains the cardiorenal syndrome in this patient?

• A Renal artery stenosis causing prerenal azotemia
• B Reduced cardiac output causing decreased renal perfusion with neurohormonal activation ✓
• C Nephrotoxic effect of ACE inhibitors causing acute tubular necrosis
• D Postrenal obstruction from prostatic hypertrophy

Explanation

Cardiorenal syndrome type 1 (acute) or type 2 (chronic) results from reduced cardiac output leading to decreased renal perfusion pressure, activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and venous congestion. This causes sodium and water retention and progressive renal dysfunction. The low sodium and rising creatinine with high BNP reflect this pathophysiology. While ACE inhibitors can worsen renal function, they are not nephrotoxic in the sense of causing tubular necrosis.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.