期刊文献+

糖尿病肾病的尿微量白蛋白监测及药物预防作用的的研究

Study of Preventive Effect of ACEI on Diabetic Nephropathy and Monitoring of Urinary Micro-albumin
下载PDF
导出
摘要 目的:对Ⅱ型糖尿病患者进行长期尿微量白蛋白监测,观察血管紧张素转换酶抑制剂(ACEI)预防糖尿病肾病(DN)的作用。方法:对象为尿微白蛋白<30mg/24Ⅱ型糖尿病患者。血压正常治疗组27人,给予卡托普利,高血压治疗组15人,在其它抗高血压治疗的基础上加用卡托普利,同时设没有使用卡托普利的对照组病人。每3个月检查一次尿微白蛋白。结果:长达33个月~54个月的观察,血压正常者治疗组有6例(6/27)转为微白蛋白尿,无1例发展为临床白蛋白尿,对照组4例(4/27)转为微白蛋白尿,1例(1/27)转为临床白蛋白尿,P=0.49;高血压治疗组有1例(1/15)转为微蛋白尿,对照组3例(3/15)转为微白蛋白尿,P=0.28。上述治疗组与对照组结果比较均无显著性差异(P>0.05)。结论:ACEI不能阻止糖尿病患者微白蛋白尿形成和不能预防DN的发生。 To study the preventive effect of an angiotensin-converting enzyme inhibitor (ACEI) on type 2 diabetic nephropathy (DN) using urinary micro-albumin as a marker. Methods: Two groups of type 2 diabetes with urinary micro-albumin<30mg/24h were entered for this study, normal blood pressure given captopril (n= 27) and without captopril served as control (n=27); hypertension treated with anti-hypertension preparations and captopril (n=15), also without captopril served as control (n=15). Urinary micro-albumin were monitored every three months. Results: During the 33-54 months of observation, in normal blood pressure group, 6 cases (6/27) of patients taken captopril developed micro-albuminuria, none developed clinical albuminuria; 4 cases (4/27) of controls developed micro-albuminuria, with one case become clinical albuminuria (p=0.49). In hypertension group, 1 case only (1/15) in captopril treated patients and 3 cases (3/15) of controls developed micro-albuminuria (p=0.28). Conclusion: ACEI might have no preventing effect on developing of DN and micro-albuminuria.
出处 《伤残医学杂志》 2003年第4期46-48,共3页 Medical Journal of Trauma and Disability
关键词 糖尿病肾病 尿微量白蛋白 血管紧张素转换酶抑制剂 糖尿病 微血管并发症 Diabetic nephropathy Preventive ACEI Urinary micro-albumin
  • 相关文献

参考文献3

二级参考文献13

  • 1丁鹤林.接近正常的血糖对糖尿病微血管并发症的影响[J].国外医学(内科学分册),1995,22(9):373-376. 被引量:17
  • 21,Krolewski AS. Geneticsof diabetic nephropathy:evidence for major and minor gene effects. Kidney Int,1999,55:1582~1596.
  • 32,Rogus JJ,Krolewski AS. Using discordant sib-pairs to map loci for qualitative traitswith high sibling recurrence risk. Am J Hum Genet,1996,59:1376~1381.
  • 43,Faronato PP,Maioli M,Tonolo G,et al. Clustering of albumin excretion rateabnormalities in Caucasian patients with NIDDM:the Italy NIDDM nephropathy study group.Diabetologia,1997,40:816~823.
  • 54,Krolewski M,Eggers P,Warram JH,et al. Magnitude of end-stage renal disease in IDDM:a35 year follow-up study. Kidney Int,1996,50:2041~2046.
  • 66,Maoczulski DK,Rogus JJ,Antonellis A,et al. Major susceptibility locus for nephropathyin type-1 diabetes mellitus on chromosome 3q:results of novel discordant sib-pairanalysis. Diabetes,1998,47:1164~1169.
  • 77,Rogus JJ,Moczulski DK,Freire MB,et al. Diabetic nephropathy is associated with AGTpolymorphism T235:results of a family-based study. Hypertension,1998,31:627~631.
  • 88,Imperatore G,Hanson RL,Pettitt DJ,et al. Sib-pair linkage analysis for susceptibilitygenes for microvascular complications among Pima Indians with type-2 diabetes millitus.Diabetes,1998,47:821~830.
  • 99,Anderson S. Role of local and systemic angiotensin in diabetic renal disease. KidneyInt,1999,52(suppl. 63):S107~S110.
  • 1010,Border WA,Noble NA. Evidence that TGF-β should be a therapeutic target in diabeticnephropathy. Kidney Int,1999,54:1390~1391.

共引文献33

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部