A patient with hypertension and CKD with proteinuria is started on an ACE inhibitor. The reno-protective mechanism of ACEi in diabetic nephropathy, beyond blood pressure lowering, primarily involves:

• A Dilation of the afferent arteriole, reducing glomerular capillary pressure
• B Preferential dilation of the efferent arteriole, reducing intraglomerular hypertension ✓
• C Direct inhibition of mesangial cell proliferation via bradykinin
• D Reducing tubular proteinuria by blocking megalin-mediated endocytosis

Explanation

In diabetic nephropathy, intraglomerular hypertension is a key driver of progression. Angiotensin II preferentially constricts the efferent arteriole (which has greater angiotensin II sensitivity than the afferent arteriole), thereby maintaining high glomerular capillary pressure. ACE inhibitors reduce angiotensin II, causing preferential efferent dilation, dropping intraglomerular pressure and proteinuria irrespective of systemic BP changes. This hemodynamic effect is central to nephroprotection. Option A would worsen proteinuria; options C and D are not the primary mechanisms.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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