EFFECT OF CAPTOPRIL ON PROGRESSION TO CLINICAL PROTEINURIA IN PATIENTS WITH INSULIN-DEPENDENT DIABETES-MELLITUS AND MICROALBUMINURIA

Citation
G. Viberti et al., EFFECT OF CAPTOPRIL ON PROGRESSION TO CLINICAL PROTEINURIA IN PATIENTS WITH INSULIN-DEPENDENT DIABETES-MELLITUS AND MICROALBUMINURIA, JAMA, the journal of the American Medical Association, 271(4), 1994, pp. 275-279
Citations number
39
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medicine, General & Internal
ISSN journal
0098-7484
Volume
271
Issue
4
Year of publication
1994
Pages
275 - 279
Database
ISI
SICI code
0098-7484(1994)271:4<275:EOCOPT>2.0.ZU;2-J
Abstract
Objectives.-To study the effect of angiotensin converting enzyme inhib ition on the rate of progression to clinical proteinuria and the rate of change of albumin excretion rates in patients with insulin-dependen t diabetes mellitus and persistent microalbuminuria. Design and Settin g.-Randomized, double-blind, placebo-controlled clinical trial of 2 ye ars' duration at 12 hospital-based diabetes centers. Patients.-Ninety- two patients with insulin-dependent diabetes mellitus and persistent m icroalbuminuria but no hypertension. Intervention.-The patients were r andomly allocated in blocks of two to receive either captopril, 50 mg, or placebo twice per day. Measurements.-Albumin excretion rate, blood pressure, glycosylated hemoglobin level, and fructosamine level every 3 months; urinary urea nitrogen excretion every 6 months; and glomeru lar filtration rate every 12 months. Results.-Twelve patients receivin g placebo and four receiving captopril progressed to clinical proteinu ria, defined as an albumin excretion rate persistently greater than 20 0 mug/min and at least a 30% increase from baseline (P=.05). The proba bility of progression to clinical proteinuria was significantly reduce d by captopril therapy (P=.03 by log-rank test Albumin excretion rate rose from a geometric mean (95% confidence interval) of 52 (39 to 68) to 76 (47 to 199) mug/min in the placebo group but fell from 52 (41 to 65) to 41 (28 to 60) mug/min in the captopril group, a significant di fference (P<.01). Mean blood pressure was similar at baseline in the t wo groups and remained unchanged in the placebo group but fell signifi cantly, by 3 to 7 mm Hg, in the captopril group. Glycosylated hemoglob in levels and glomerular filtration rate remained stable in the two gr oups. Conclusions.-Captopril therapy significantly impeded progression to clinical proteinuria and prevented the increase in albumin excreti on rate in nonhypertensive patients with insulin-dependent diabetes me llitus and persistent microalbuminuria.