Mathiesen E R, Hommel E, Giese J, Parving H H
Hvidøre Hospital, Klampenborg, Denmark.
BMJ. 1991 Jul 13;303(6794):81-7. doi: 10.1136/bmj.303.6794.81.
To assess the effectiveness of angiotensin converting enzyme inhibition in preventing the development of diabetic nephropathy (albuminuria greater than 300 mg/24h).
Open randomised controlled study of four years' duration.
Outpatient diabetic clinic in tertiary referral centre.
44 normotensive (mean blood pressure 127/78 (SD 12/10) mm Hg) insulin dependent diabetic patients with persistent microalbuminuria (30-300 mg/24h).
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.
Albuminuria, kidney function, development of diabetic nephropathy (albuminuria greater than 300 mg/24 h), and arterial blood pressure.
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.
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.
评估血管紧张素转换酶抑制剂在预防糖尿病肾病(蛋白尿超过300mg/24小时)发生方面的有效性。
为期四年的开放性随机对照研究。
三级转诊中心的门诊糖尿病诊所。
44名血压正常(平均血压127/78(标准差12/10)mmHg)的胰岛素依赖型糖尿病患者,伴有持续性微量蛋白尿(30 - 300mg/24小时)。
治疗组(n = 21)最初给予卡托普利(25mg/24小时)。在最初16个月内剂量增加至100mg/24小时,30个月后加用噻嗪类药物。其余23名患者未接受治疗。
蛋白尿、肾功能、糖尿病肾病(蛋白尿超过300mg/24小时)的发生情况以及动脉血压。
基线时临床和实验室变量具有可比性。卡托普利治疗组尿白蛋白排泄量从82(66 - 106)逐渐降至57(39 - 85)mg/24小时(几何均数(95%置信区间)),而对照组则从105(77 - 153)增至166(83 - 323)mg/24小时(p < 0.05)。未治疗的患者中有7例进展为糖尿病肾病,而卡托普利治疗组患者无一例发生临床显性糖尿病肾病(p < 0.05)。两组的全身血压、肾小球滤过率、糖化血红蛋白浓度以及尿钠和尿素排泄量基本保持不变。
研究结果表明,血管紧张素转换酶抑制剂可延缓血压正常的胰岛素依赖型糖尿病伴持续性微量蛋白尿患者临床显性糖尿病肾病的发生。