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

Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria
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DOI:
10.1016/s0140-6736(98)10363-x
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发表时间:
1999-07-31
期刊:
影响因子:
168.9
通讯作者:
Remuzzi, G
Remuzzi, G
中科院分区:
医学1区
文献类型:
--
作者:
Ruggenenti, P;Perna, A;Remuzzi, G

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研究背景雷米普利对肾病疗效(REIN)研究的第2层已经表明,在慢性肾病和每24小时蛋白尿3g或更多的患者中,血管紧张素转换酶(ACE)抑制降低了肾小球滤过率下降的速度,并将在REIN第1层中发现的血清肌酐翻倍或终末期肾功能衰竭(ESRF)的综合风险减半,在REIN第1层中发现了安慰剂加传统降压药的对照组。方法在这项双盲试验的第1层,186例患者被随机分为雷米普利组和对照组(安慰剂加常规降压治疗),目标是使舒张压低于90 mm Hg。主要终点是肾小球滤过率(GFR)和达到终末期肾功能衰竭或显性蛋白尿的时间(大于或等于3g/24小时)。中位随访期为31个月,平均每月肾小球滤过率下降无显著差异(雷米普利0.26[SE 0.05]毫升/分钟1.73米(2),对照组0.29[0.06]毫升/分钟)。雷米普利组进展为终末期肾衰的发生率(9/99比18/87)显著减少,相对危险度(RR)为2.72(95%可信区间1.22-6.08);进展为显性蛋白尿(15/99比27/87,RR 2.40[1.27-4.52])。基线GFR在45mL/min/1.73m(2)或以下,蛋白尿在1.5g/24 h或以上的患者病情进展更快,从雷米普利治疗中获益最多。雷米普利组尿蛋白减少了13%,对照组增加了15%。心血管事件相似。正如预期的那样,第一层的GFR下降率和ESRF的频率比第二层低得多。解释说,在非糖尿病肾病中,ACE抑制甚至对非肾病蛋白尿的患者也具有肾脏保护作用。
Background Stratum 2 of the Ramipril Efficacy in Nephropathy (REIN) study has already shown that in patients with chronic nephropathies and proteinuria of 3 g or more per 24 h, angiotensin-converting enzyme (ACE) inhibition reduced the rate of decline in glomerular filtration and halved the combined risk of doubling of serum creatinine or end-stage renal failure (ESRF) found in controls on placebo plus conventional antihypertensives, In REIN stratum 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 randomised to a ramipril or a control (placebo plus conventional antihypertensive therapy) 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 (ramipril 0.26 [SE 0.05] mL per min per 1.73 m(2), control 0.29 [0.06]). Progression to ESRF was significantly less common in the ramipril group (9/99 vs 18/87) for a relative risk (RR) of 2.72 (95% CI 1.22-6.08); so was progression to overt proteinuria (15/99 vs 27/87, RR 2.40 [1.27-4.52]). Patients with 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 treatment. 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 renoprotection even to patients with non-nephrotic proteinuria.