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The AIPRI Study. The AIPRI Study ACE Inhibition in Progressive Renal Insufficiency. Reference Maschio G, Alberti D, Locatelli F, et al . Angiotensin-converting enzyme inhibitors and kidney protection: the AIPRI trial. J Cardiovasc Pharmacol. 1999;33(Suppl.1):S16–S20; discussion S41—S43.
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The AIPRI Study ACE Inhibition in Progressive Renal Insufficiency Reference Maschio G, Alberti D, Locatelli F, et al. Angiotensin-converting enzyme inhibitors and kidney protection: the AIPRI trial. J Cardiovasc Pharmacol. 1999;33(Suppl.1):S16–S20; discussion S41—S43.
Background Angiotensin-converting enzyme (ACE) inhibitors have renoprotective effect as shown in the recent trials in both diabetic and non-diabetic patients. This property is independent of blood pressure control.
Aim To determine whether a non-sulfhydryl ACE inhibitor, benazepril, was safe and effective in slowing progression of functional renal deterioration in patients with renal disease of various origins and mild to moderate chronic renal failure (CRF).
Summary of Key Results • In patients with mild CRF: 5 patients of 120 of benazepril group and 15 of 107 patients in placebo group reached endpoints. • In patients with moderate CRF: 26 patients of 180 of benazepril group and 42 of 17 6 patients in placebo group reached endpoints.
Protective effect of benazepril was greater in patients with proteinuria of more than 3 g/24 h than in those with proteinuria of 1.0–3.0 g/24 h at randomization. • Greater increase in SCr concentration was observed in the benazepril groups of both strata during the first 3 months of treatment. • SCr concentrations in the benazepril groups increased less than those in the placebo groups and were more evident in patients with mild CRF (Fig. 3). • In comparison with baseline, diastolic blood pressure decreased by 3.5–4.0 mm Hg in the benazepril group and increased by 0.2–1.5 mm Hg in the placebo group. • A clinically relevant decrease in urine protein excretion was observed in benazepril-treated patients.
Conclusion Significant renoprotective effect of benazepril was seen in patients with glomerulonephritis, in those with renal failure of unknown origin, and in the small group of patients with diabetic nephropathy. It was effective in slowing the rate of progression of renal disease and improving the renal survival in patients with CRF of non-diabetic origin and was more protective in patients with proteinuric than non-proteinuric renal disease. Benazepril is effective in slowing the rate of progression and improving the survival of renal function in patients with renal diseases of various origins. This protective effect is associated with a clinically relevant decrease in both blood pressure and proteinuria.