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正常血压的II型糖尿病伴持续性轻度蛋白尿患者的血管紧张素转换酶抑制作用

Angiotensin converting enzyme inhibition in normotensive type II diabetics with persistent mild proteinuria.

作者信息

Stornello M, Valvo E V, Scapellato L

机构信息

Centro per lo studio e la terapia dell'Ipertensione, Ospedale Generale Umberto l, Syracuse, Italy.

出版信息

J Hypertens Suppl. 1989 Dec;7(6):S314-5. doi: 10.1097/00004872-198900076-00153.

Abstract

To evaluate the effect of enalapril on proteinuria, 16 normotensive type II diabetics with persistent proteinuria were studied. At random, the patients were allocated to enalapril (5 mg once a day) or placebo, in a double-blind fashion, for 12 months. Blood pressure, heart rate, urinary albumin excretion, plasma renin activity and aldosterone, blood glucose, serum fructosamine, urine urea and body weight were checked monthly during the run-in period and every 2 months during the treatment period. The kidney function was studied at the beginning of the study and during the sixth and 12th months. Enalapril decreased urinary albumin excretion in our patients in the absence of any effect on blood pressure and kidney function. Our data may be interpreted on the basis of a direct vascular effect of enalapril that is probably related to a tissue mechanism consisting of reduced angiotensin formation, increased kinins, or both, or of other unknown factors.

摘要

为评估依那普利对蛋白尿的影响,我们对16例患有持续性蛋白尿的血压正常的II型糖尿病患者进行了研究。患者被随机双盲分配至依那普利组(每日一次,每次5毫克)或安慰剂组,治疗12个月。在导入期每月检查血压、心率、尿白蛋白排泄、血浆肾素活性和醛固酮、血糖、血清果糖胺、尿尿素和体重,在治疗期每2个月检查一次。在研究开始时以及第6个月和第12个月时研究肾功能。依那普利在对血压和肾功能无任何影响的情况下降低了我们患者的尿白蛋白排泄。我们的数据可以基于依那普利的直接血管效应来解释,这可能与一种组织机制有关,该机制包括减少血管紧张素形成、增加激肽或两者兼有,或者与其他未知因素有关。

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