Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria

Citation
P. Ruggenenti et al., Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria, LANCET, 354(9176), 1999, pp. 359-364
Citations number
18
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
LANCET
ISSN journal
01406736 → ACNP
Volume
354
Issue
9176
Year of publication
1999
Pages
359 - 364
Database
ISI
SICI code
0140-6736(19990731)354:9176<359:RPOAIN>2.0.ZU;2-I
Abstract
Background Stratum 2 of the Ramipril Efficacy in Nephropathy (REIN) study h as already shown that in patients with chronic nephropathies and proteinuri a of 3 g or more per 24 h, angiotensin-converting enzyme (ACE) inhibition r educed the rate of decline in glomerular filtration and halved the combined risk of doubling of serum creatinine or end-stage renal failure (ESRF) fou nd in controls on placebo plus conventional antihypertensives, In REIN stra tum 1, reported here, 24 h proteinuria was Ig or more but less than 3 g per 24 h. Methods In stratum 1 of this double-blind trial 186 patients were randomise d to a ramipril or a control (placebo plus conventional antihypertensive th erapy) group targeted at achieving a diastolic blood pressure of less than 90 mm Hg. The primary endpoints were change in glomerular filtration rate ( GFR) and time to ESRF or overt proteinuria (greater than or equal to 3 g/24 h). Median follow-up was 31 months. Findings The decline in GFR per month was not significantly different (rami pril 0.26 [SE 0.05] mL per min per 1.73 m(2), control 0.29 [0.06]). Progres sion to ESRF was significantly less common in the ramipril group (9/99 vs 1 8/87) for a relative risk (RR) of 2.72 (95% CI 1.22-6.08); so was progressi on to overt proteinuria (15/99 vs 27/87, RR 2.40 [1.27-4.52]). Patients wit h a baseline GFR of 45 mL/min/1.73 m(2) or less and proteinuria of 1.5 g/24 h or more had more rapid progression and gained the most from ramipril tre atment. Proteinuria decreased by 13% in the ramipril group and increased by 15% in the controls. Cardiovascular events were similar. As expected, the rate of decline in GFR and the frequency of ESRF were much lower in stratum 1 than they had been in stratum 2. Interpretation In non-diabetic nephropathies, ACE inhibition confers renopr otection even to patients with non-nephrotic proteinuria.