Association between genetic polymorphism of the angiotensin-converting enzyme and diabetic nephropathy: a meta-analysis comprising 26,580 subjects

• Published in: Journal of the renin-angiotensin-aldosterone system Vol. 13; no. 1; pp. 161 - 174
• Main Authors: Wang, Furu, Fang, Qiaoqiao, Yu, Ningle, Zhao, Deyu, Zhang, Yimei, Wang, Jin, Wang, Quan, Zhou, Xianfeng, Cao, Xingjiang, Fan, Xiangyong
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.03.2012
• Subjects: Adult; Aged; Diabetic Nephropathies - enzymology; Diabetic Nephropathies - genetics; Genetic Association Studies; Genetic Heterogeneity; Genetic Predisposition to Disease; Humans; INDEL Mutation - genetics; Middle Aged; Models, Genetic; Odds Ratio; Peptidyl-Dipeptidase A - genetics; Polymorphism, Genetic; Publication Bias; polymorphism; ACE I/D; diabetic nephropathy; DM type; genetic epidemiology
• ISSN: 1470-3203; 1752-8976; 1752-8976
• DOI: 10.1177/1470320311417655

Introduction: The effect of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism on risk of diabetic nephropathy (DN) is still conflicting. The present meta-analysis was performed to evaluate the overall risk of this polymorphism associated with DN in different groups. Materials and methods: A predefined search was performed on 14,108 DN cases and 12,472 controls from 63 published studies by searching electronic databases and reference lists of relevant articles. Results: In this meta-analysis, we found a significant association between the ACE I/D polymorphism and the risk of DN for all genetic models (ID versus II: odds ratio [OR] = 1.12, 95% confidence interval [CI] 1.02–1.24; DD versus II: OR = 1.27, 95% CI 1.13–1.44; allele contrast: OR = 1.15, 95% CI 1.08–1.23; dominant model: OR = 1.18, 95% CI 1.07–1.31; and recessive model: OR = 1.18, 95% CI 1.08–1.30, respectively). In stratified analysis by ethnicity and DM type, we further found that the Asian group with type 2 diabetes mellitus (T2DM) showed a significant association for all genetic models (ID versus II: OR = 1.25, 95% CI 1.07–1.47; DD versus II: OR = 1.57, 95% CI 1.24–1.98; allele contrast: OR = 1.30, 95% CI 1.15–1.46; dominant model: OR = 1.37, 95% CI 1.10–1.69; and recessive model: OR = 1.34, 95% CI 1.15–1.56, respectively). Conclusions: Our study suggested that the ACE I/D polymorphism may contribute to DN development, especially in the Asian group with T2DM.