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Efficacy of captopril in postponing nephropathy in normotensive insulin dependent diabetic patients with microalbuminuria.

机译:卡托普利在血压正常的胰岛素依赖型糖尿病伴微量白蛋白尿患者中延缓肾病的疗效。

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摘要

OBJECTIVE--To assess the effectiveness of angiotensin converting enzyme inhibition in preventing the development of diabetic nephropathy (albuminuria greater than 300 mg/24h). DESIGN--Open randomised controlled study of four years' duration. SETTING--Outpatient diabetic clinic in tertiary referral centre. PATIENTS--44 normotensive (mean blood pressure 127/78 (SD 12/10) mm Hg) insulin dependent diabetic patients with persistent microalbuminuria (30-300 mg/24h). INTERVENTIONS--The treatment group (n = 21) was initially given captopril (25 mg/24 h). The dose was increased to 100 mg/24 h during the first 16 months and thiazide was added after 30 months. The remaining 23 patients were left untreated. MAIN OUTCOME MEASURES--Albuminuria, kidney function, development of diabetic nephropathy (albuminuria greater than 300 mg/24 h), and arterial blood pressure. RESULTS--Clinical and laboratory variables were comparable at baseline. Urinary excretion of albumin was gradually reduced from 82 (66-106) to 57 (39-85) mg/24 h (geometric mean (95% confidence interval)) in the captopril treated group, whereas an increase from 105(77-153) to 166 (83-323) mg/24 h occurred in the control group (p less than 0.05). Seven of the untreated patients progressed to diabetic nephropathy, whereas none of the captopril treated patients developed clinical overt diabetic nephropathy (p less than 0.05). Systemic blood pressure, glomerular filtration rate, haemoglobin A1c concentration, and urinary excretion of sodium and urea remained practically unchanged in the two groups. CONCLUSIONS--The findings suggest that angiotensin converting enzyme inhibition postpones the development of clinical overt diabetic nephropathy in normotensive insulin dependent diabetic patients with persistent microalbuminuria.
机译:目的-评估血管紧张素转化酶抑制在预防糖尿病性肾病(白蛋白尿大于300 mg / 24h)的发展中的有效性。设计-为期四年的开放随机对照研究。地点-三级转诊中心的门诊糖尿病诊所。患者-44血压正常(平均血压127/78(SD 12/10)mm Hg)胰岛素依赖型糖尿病患者,伴有持续性微量白蛋白尿(30-300 mg / 24h)。干预措施-治疗组(n = 21)最初接受了卡托普利(25 mg / 24 h)。在最初的16个月内剂量增加至100 mg / 24 h,并在30个月后添加噻嗪类。其余23名患者未经治疗。主要观察指标-白蛋白尿,肾功能,糖尿病性肾病的发展(白蛋白尿大于300 mg / 24 h)和动脉血压。结果-临床和实验室变量在基线时具有可比性。卡托普利治疗组的尿白蛋白排泄从82(66-106)降低至57(39-85)mg / 24 h(几何平均数(95%置信区间)),而尿白蛋白的排泄量则由105(77-153)增加)对照组的166(83-323)mg / 24 h(p小于0.05)。未治疗的患者中有七名进展为糖尿病性肾病,而卡托普利治疗的患者均未出现临床上明显的糖尿病性肾病(p小于0.05)。两组的全身血压,肾小球滤过率,血红蛋白A1c浓度以及尿钠和尿的排泄率实际上保持不变。结论-研究结果表明,在血压正常的胰岛素依赖型糖尿病伴持续性微量白蛋白尿的糖尿病患者中,血管紧张素转换酶的抑制作用会延迟临床明显的糖尿病性肾病的发展。

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