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This reply clarifies the renal mechanisms, beyond systemic blood pressure reduction, by which calcium antagonists and ACE inhibitors exert antiproteinuric effects in diabetic nephropathy.
In Reply.— It is clear that converting enzyme inhibitors reduce urinary albumin excretion through alterations in both renal hemodynamics and glomerular permselectivity.¹⁻³The mechanism, however, by which calcium antagonists reduce urinary albumin excretion is unclear. Gansevoort et al make a persuasive argument that the antiproteinuric effects of calcium antagonists are related to their antihypertensive rather than their renal effects. However, recent studies clearly document that certain classes of calcium antagonists have renal effects that help explain their antiproteinuric effects. At least three major changes occur in the kidney following a prolonged history of diabetes. First, there is expansion of the mesangial matrix. Second, there is altered glomerular permeability to albumin and other molecules secondary to alterations in charge and size selectivity of the glomerular capillary membrane. Last, there is a persistent elevation in intraglomerular capillary pressure that is sustained in theintactremnant nephrons as renal disease progresses. Clearly,
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George L. Bakris (1992) studied this question.
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