Abstract
Studies of the association between angiotensin II receptor type 1 A1166C (AGTR1 A1166C) polymorphism and chronic kidney disease (CKD) risk have yielded conflicting results. We conducted a combined case-control study and meta-analysis to better define this association. The case-control study included 634 end-stage renal disease (ESRD) patients and 739 healthy controls. AGTR1 A1166C genotype was determined using polymerase chain reaction and iPLEX Gold SNP genotyping methods. The meta-analysis included 24 studies found in the PubMed and Cochrane Library databases. Together, the case-control study and meta-analysis included 36 populations (7,918 cases and 6,905 controls). We found no association between the C allele and ESRD (case-control study: OR: 1.02, 95% CI: 0.77–1.37; meta-analysis: OR: 1.07; 95% CI: 0.97–1.18). Co-dominant, dominant, and recessive model results were also not significant. No known environmental factors moderated the effect of AGTR1 A1166C on CKD in our gene-environment interaction analysis. Sensitivity analysis showed an AGTR1 A1166C-CKD association in Indian populations (OR: 1.46, 95% CI: 1.26–1.69), but not in East Asian or Caucasian populations. Additional South Asian studies will be required to confirm the potential role of this polymorphism in CKD.
Highlights
Chronic kidney disease (CKD) is highly prevalent worldwide [1,2,3,4], and increases patient cardiovascular event and mortality risks [5]
We further analyzed the association between Ang II receptor types 1 (AGTR1) A1166C and end-stage renal disease (ESRD) after adjusting age, sex, body mass index (BMI), hypertension, diabetes mellitus (DM), and smoking, because these factors differed between controls and cases
No investigative factors moderated the effects of AGTR1 A1166C on chronic kidney disease (CKD). Both our case-control study and meta-analysis revealed no association between AGTR1 A1166C and ESRD
Summary
Chronic kidney disease (CKD) is highly prevalent worldwide [1,2,3,4], and increases patient cardiovascular event and mortality risks [5]. Genetic factors play key roles in CKD pathogenesis. Creatinine clearance appears inherited in 46% of cases [6]. Identification and evaluation of novel candidate gene polymorphisms could lead to improved CKD diagnostic accuracies and therapeutic options. The renin-angiotensin system (RAS) regulates blood pressure and electrolyte balance, and an over-active RAS leads to CKD [7]. RAS functions mainly through its final product, angiotensin II (Ang II), which binds www.impactjournals.com/oncotarget
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