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The role of ace inhibition in diabetic renal disease is clear: ACE inhibitors delay the progression from microalbuminuria (30-300 mg protein/24 hours) to proteinuria (> 300 mg/24 hours). Once overt proteinuria is established, they decrease the level of proteinuria, retard decline in GFR, and delay the onset of overt nephropathy. No such clearly defined results exist for the use of ACE inhibitors in non-diabetic renal disease.
The authors reviewed 10 randomized trials of at least one year’s duration, totalling 1594 patients. Patients receiving ACE inhibitors had a relative risk of 0.70 for end-stage renal disease. In addition, there was a significant change in systolic blood pressure (decreased 4.9 mmHg) among ACE inhibitor recipients, which is of sufficient magnitude to favorably affect progression of renal disease, though the mean change in diastolic BP (1.2 mmHg) was not clinically relevant. Although meta-analysis did show a favorable effect of ACE inhibitors on progression of renal disease, no favorable effect of such treatment on overall mortality was demonstrable.
ACE inhibitors and angiotensin II receptor blockers both share favorable effects on renal hemodynamics, including decreases in intra-glomerular pressure and suppression of mediators of glomerular hypertrophy and fibrosis. This meta-analysis would suggest that use of ACE inhibition should produce parallel favorable effects on renal dysfunction in non-diabetic patients to those already well demonstrated in diabetics.
Giatris I, et al. Ann Intern Med 1997; 127:337-345.