Association Between IL-6 Polymorphisms and Diabetic Nephropathy Risk: A Meta-analysis

Am J Med Sci. 2019 Nov;358(5):363-373. doi: 10.1016/j.amjms.2019.07.011. Epub 2019 Jul 31.

Abstract

Background: The objective of this work was to evaluate the relevance of frequent interleukin-6 (IL-6) polymorphisms and diabetic nephropathy (DN) susceptibility by a systematic meta-analysis.

Materials and methods: The included studies related to the relationship between IL-6 and DN risk were searched from Pubmed, Embase and the Cochrane Library, and the Newcastle-Ottawa Scale was used to evaluate the study quality. A heterogeneity test was performed to determine the appropriate effect models based on the Q test and I2 statistic. Odds ratios with 95% confidence intervals were used to determine the strength of associations. Afterwards, subgroup analysis was conducted to assess the effect of specific factors on the corresponding results. Additionally, publication bias and sensitivity analysis were also undertaken.

Results: In total, 11 eligible articles were obtained. The meta-analysis revealed that the "C"allele of IL-6 rs1800795 was related to the decreased risk of DN (C versus G: P = 0.0471). The "G"allele of IL-6 rs1800796 was predominately associated with higher DN risks (GG versus CC: P = 0.0194; GG versus CC + GC: P = 0.0196). The "C"allele of IL-6 rs1800797 was implicated with higher prevalence of DN (C versus G: P = 0.0001; CC versus GG: P = 0.0003; CC versus GG + CG: P = 0.0227; CC + CG versus GG: P = 0.0001) while IL-6 rs2069837 and rs2069840 were not correlated with the susceptibility to DN.

Conclusions: This meta-analysis indicated that IL-6 rs1800795, rs1800796 and rs1800797 played important roles in DN development while IL-6 rs2069837 and rs2069840 might not be related to DN.

Keywords: Diabetic nephropathy; Heterogeneity; IL-6 polymorphisms; Meta-analysis; Publication bias; Sensitivity analysis.

Publication types

  • Meta-Analysis

MeSH terms

  • Diabetic Nephropathies / genetics*
  • Genetic Predisposition to Disease
  • Humans
  • Interleukin-6 / genetics*
  • Polymorphism, Single Nucleotide

Substances

  • IL6 protein, human
  • Interleukin-6