A patient with bilateral renal artery stenosis is placed on an ACE inhibitor. The acute deterioration in renal function occurs because:
- A Angiotensin II normally maintains GFR by preferentially constricting the efferent arteriole; its blockade reduces glomerular filtration pressure ✓
- B ACE inhibitors reduce systemic blood pressure below the autoregulatory range
- C ACE inhibitors reduce aldosterone, causing hyponatremia that impairs tubular function
- D ACE inhibitors directly reduce renal prostaglandin synthesis
Explanation
In bilateral renal artery stenosis, GFR is maintained by angiotensin II-mediated efferent arteriolar constriction, which preserves glomerular hydrostatic pressure despite reduced renal perfusion pressure. ACE inhibitors abolish this compensatory efferent constriction, causing a precipitous fall in intraglomerular pressure and GFR. This is a classic clinical correlation of tubuloglomerular feedback and angiotensin physiology. Systemic hypotension may contribute but is not the primary mechanism.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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