Hay U, Ludvik B, Gisinger C, Schernthaner G
II. Medizinische Universitätsklinik, Universität Wien.
Schweiz Med Wochenschr. 1988 Feb 6;118(5):165-9.
The effect of angiotensin converting enzyme inhibition with captopril therapy (3 x 12.5 mg/d) on heavy proteinuria and kidney function was investigated in 10 insulin-treated diabetic patients over a period of 6 months. Urinary protein excretion increased from 3706 mg/day (SD 1491) to 5405 (SD 2699) after 6 months of treatment (p = 0.05); serum creatinine rose from 248 mumol/l (SD 163) to 283 (SD 186) (p less than 0.01), whereas there was no significant difference in blood pressure before (150/80 mm Hg--SD 23/6) and after therapy (150/90 mm Hg--SD 23/10). HbA1c as a marker of metabolic long-term control decreased from 8.3% (SD 1.0) to 7.3% (SD 1.0) (p less than 0.05). No beneficial effects of low dose angiotensin converting enzyme inhibition on heavy proteinuria could be demonstrated in this group of patients with advanced diabetic nephropathy. In particular, progressive deterioration of kidney function was not influenced by the captopril treatment. In diabetic patients with incipient diabetic nephropathy presenting with microalbuminuria, further studies concerning a possible therapeutic effect are necessary.
在10例接受胰岛素治疗的糖尿病患者中,研究了卡托普利疗法(3×12.5毫克/天)抑制血管紧张素转换酶对重度蛋白尿和肾功能的影响,为期6个月。治疗6个月后,尿蛋白排泄量从3706毫克/天(标准差1491)增至5405(标准差2699)(p = 0.05);血清肌酐从248微摩尔/升(标准差163)升至283(标准差186)(p<0.01),而治疗前(150/80毫米汞柱——标准差23/6)和治疗后(150/90毫米汞柱——标准差23/10)的血压无显著差异。作为代谢长期控制指标的糖化血红蛋白从8.3%(标准差1.0)降至7.3%(标准差1.0)(p<0.05)。在这组晚期糖尿病肾病患者中,未证实低剂量血管紧张素转换酶抑制对重度蛋白尿有有益作用。特别是,卡托普利治疗并未影响肾功能的进行性恶化。对于出现微量白蛋白尿的早期糖尿病肾病患者,有必要进一步研究其可能的治疗效果。