Abstract

Background The connection between angiotensin-converting enzyme insertion/deletion (ACE I/D) gene polymorphisms and IgA nephropathy (IgAN) was conflicting. This pooled analysis was performed to explore this issue. Methods All eligible investigations were identified from various electronic databases, and the pooled analysis was evaluated using Stata software. Results 27 studies with 2538 IgAN cases and 3592 controls were included. In overall subjects, ACE D allele, DD, and II genotype were associated with IgAN susceptibility (D vs. I: OR = 1.21, 95% CI: 1.10–1.32, P < 0.001; DD vs. ID + II: OR = 1.38, 95% CI: 1.20–1.60, P < 0.001; and II vs. DD + ID: OR = 0.83, 95% CI: 0.73–0.95, P=0.007). In Asian and Chinese patients, ACE I/D gene polymorphism was also correlated with IgAN vulnerability. Moreover, ACE D allele, DD, and II genotype were correlated with the progression of IgAN (D vs. I: OR = 1.37, 95% CI: 1.09–1.73, P=0.008; DD vs. ID + II: OR = 1.57, 95% CI: 1.06–2.31, P=0.024; and II vs. DD + ID: OR = 0.69, 95% CI: 0.49–0.99, P=0.045). Conversely, in Caucasian subjects, there was no link between ACE I/D gene polymorphism and the risk of IgAN. Conclusion ACE I/D gene polymorphism was correlated with the vulnerability and progression of IgAN in Asian and Chinese patients, and ACE D allele and DD homozygote genotype could be adverse factors for IgAN, while the II homozygote genotype could be an advantage factor. But, no significant association was found between ACE I/D gene polymorphism and IgAN in Caucasians.

Highlights

  • IgA nephropathy (IgAN) is a common type of glomerulonephritis globally; in the Pacific Asian region, the prevalence rate of IgAN is even more high [1]

  • Some research studies have demonstrated that angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphism would affect the vulnerability of IgAN [8,9,10]

  • Our study demonstrated that the Angiotensin-converting enzyme (ACE) I/D polymorphism was associated with the susceptibility and progression of IgAN

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Summary

Introduction

IgA nephropathy (IgAN) is a common type of glomerulonephritis globally; in the Pacific Asian region, the prevalence rate of IgAN is even more high [1]. It is a serious public health problem with very high mortality and morbidity, and recent studies have showed that approximately 20% IgAN patients would progress to endstage renal disease (ESRD) if lacking effective treatment [2]. Some research studies have demonstrated that ACE I/D polymorphism would affect the vulnerability of IgAN [8,9,10]

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