Abstract

Chronic renal disease evolves to end-stage renal failure through events, including enhanced intraglomerular pressure and plasma protein ultrafiltration, mediated at least in part by angiotensin II. Angiotensin-converting enzyme inhibitors reduce intracapillary pressure and ameliorate glomerular size-selective function, which may account for their antiproteinuric effect and renoprotective potential. Thus, the Ramipril Efficacy in Nephropathy study found a significant correlation between enhanced urinary protein excretion and faster disease progression in non-diabetic patients with proteinuric chronic renal disease. In proteinuric non-diabetic renal disease at comparable levels of blood pressure control, angiotensin-converting enzyme inhibitors reduce proteinuria and slow disease progression to end-stage renal failure safely and more effectively than non-angiotensin-converting enzyme therapy. On the contrary, most non-proteinuric chronic renal diseases progress slowly and do not benefit specifically from angiotensin-converting enzyme inhibition therapy.

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