THE EFFECT OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ON DIABETIC NEPHROPATHY
THE EFFECT OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ON DIABETIC NEPHROPATHY
复制标题
DOI：
10.1056/nejm199311113292004
复制
发表时间：
1993-11-11
影响因子：
158.5
通讯作者：
ROHDE, RD
中科院分区：
文献类型：
--
作者：
LEWIS, EJ;HUNSICKER, LG;ROHDE, RD
背景糖尿病肾病患者肾功能进行性下降，降压药物可减缓肾功能下降。本研究的目的是确定在糖尿病肾病患者中，卡托普利是否具有独立于其对血压的影响的肾脏保护特性。我们进行了一项随机对照试验，在尿蛋白排泄量大于或等于500 mg/d且血清肌酐浓度小于或等于2.5 mg/dl（221 mumol/L）的胰岛素依赖型糖尿病患者中比较了卡托普利与安慰剂。血压目标被定义为在三年的中位随访期间实现控制。主要终点是基线血清肌酐浓度加倍。207例患者接受了卡托普利，202例患者接受了安慰剂。与安慰剂组的43例患者相比，卡托普利组的25例患者血清肌酐浓度加倍（P = 0.007）。血清肌酐浓度加倍的风险在卡托普利组总体上降低了48%，在基线血清肌酐浓度为2.0 mg/dl的亚组中降低了76（177 μ mol/L），浓度为1.5 mg/dl的亚组中为55%浓度为1.0毫克/分升（88.4 μ mol/L）的亚组中为17%。肌酐清除率的平均（+/- SD）下降率在卡托普利组为每年11 +/-21%，在安慰剂组为每年17 +/-20%（P = 0.03）。在基线血清肌酐浓度大于或等于1.5 mg/dl的患者中，卡托普利组肌酐清除率以每年23 ± 25%的速度下降，安慰剂组以每年37 ± 25%的速度下降（P = 0.01）。Captopril治疗与死亡、透析和移植联合终点风险降低50%相关，这与两组间血压的微小差异无关。Captopril可防止胰岛素依赖型糖尿病肾病患者肾功能恶化，且比单独控制血压更有效。
Background. Renal function declines progressively in patients who have diabetic nephropathy, and the decline may be slowed by antihypertensive drugs. The purpose of this study was to determine whether captopril has kidney-protecting properties independent of its effect on blood pressure in diabetic nephropathy.Methods. We performed a randomized, controlled trial comparing captopril with placebo in patients with insulin-dependent diabetes mellitus in whom urinary protein excretion was greater-than-or-equal-to 500 mg per day and the serum creatinine concentration was less-than-or-equal-to 2.5 mg per deciliter (221 mumol per liter). Blood-pressure goals were defined to achieve control during a median follow-up of three years. The primary end point was a doubling of the base-line serum creatinine concentration.Results. Two hundred seven patients received captopril, and 202 placebo. Serum creatinine concentrations doubled in 25 patients in the captopril group, as compared with 43 patients in the placebo group (P = 0.007). The associated reductions in risk of a doubling of the serum creatinine concentration were 48 percent in the captopril group as a whole, 76 percent in the subgroup with a baseline serum creatinine concentration of 2.0 mg per deciliter (177 mumol per liter), 55 percent in the subgroup with a concentration of 1.5 mg per deciliter (133 mumol per liter), and 17 percent in the subgroup with a concentration of 1.0 mg per deciliter (88.4 mumol per liter). The mean (+/- SD) rate of decline in creatinine clearance was 11 +/- 21 percent per year in the captopril group and 17 +/- 20 percent per year in the placebo group (P = 0.03). Among the patients whose base-line serum creatinine concentration was greater-than-or-equal-to 1.5 mg per deciliter, creatinine clearance declined at a rate of 23 +/- 25 percent per year in the captopril group and at a rate of 37 +/- 25 percent per year in the placebo group (P = 0.01). Captopril treatment was associated with a 50 percent reduction in the risk of the combined end points of death, dialysis, and transplantation that was independent of the small disparity in blood pressure between the groups.Conclusions. Captopril protects against deterioration in renal function in insulin-dependent diabetic nephropathy and is significantly more effective than blood-pressure control alone.