Tanvir Chowdhury Turin
- Japan Epidemiological Association
- Journal of Epidemiology (ISSN:09175040)
- pp.JE20200540, (Released:2021-02-20)
Background: Inflammation is thought to be a risk factor for kidney disease. However, discussion is controversial whether inflammatory status is either a cause or an outcome of chronic kidney disease. We aimed to investigate the causal relationship between high-sensitivity C-reactive protein (hs-CRP) and estimated glomerular filtration rate (eGFR) using mendelian randomization (MR) approaches.Methods: A total of 10,521 participants of the Japan Multi-institutional Collaborative Cohort Study was analyzed in this study. We used two-sample MR approaches (the inverse-variance weighted (IVW), the weighted median (WM), and the MR-Egger method) to estimate the effect of genetically determined hs-CRP on kidney function. We selected four and three hs-CRP associated single nucleotide polymorphisms (SNPs) as two instrumental variables (IV): IVCRP and IVAsian, based on SNPs previously identified in European and Asian populations. IVCRP and IVAsian explained 3.4% and 3.9% of the variation in hs-CRP, respectively.Results: Using the IVCRP, genetically determined hs-CRP was not significantly associated with eGFR in the IVW and the WM methods (estimate per 1 unit increase in ln(hs-CRP), 95%CI: 0.000, –0.019 to 0.020 and –0.003, –0.019 to 0.014). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 95% CI: –0.005, –0.020 to 0.010 and –0.004, –0.020 to 0.012). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: –0.008, –0.058 to 0.042; IVAsian: 0.001, –0.036 to 0.036).Conclusions: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.