日本語フィールド
著者：*Fujii R, Hishida A, Nishiyama T, Nakatochi M, Matsuo K, Ito H, Nishida Y, Shimanoe C, Nakamura Y, Turin TC, Suzuki S, Watanabe M, Ibusuki R, Takezaki T, Mikami H, Nakamura Y, Ikezaki H, Murata M, Kuriki K, Kuriyama N, Matsui D, Arisawa K, Katsuura-Kamano S, Tsukamoto M, Tamura T, Kubo Y, Kondo T, Momozawa Y, Kubo M, Takeuchi K, Wakai K題名：Assessing the Relationship Between High-sensitivity C-reactive Protein and Kidney Function Employing Mendelian Randomization in the Japanese Community-based J-MICC Study発表情報：J Epidemiol 巻: 32 号: 11 ページ: 483-488キーワード：Mendelian randomization study; eGFR; genetic epidemiology; hs-CRP; inflammation概要：Background: Inflammation is thought to be a risk factor for kidney disease. However, whether inflammatory status is either a cause or an outcome of chronic kidney disease remains controversial. 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), 0.000; 95% confidence interval [CI], -0.019 to 0.020 and -0.003; 95% CI, -0.019 to 0.014, respectively). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 0.005; 95% CI, -0.020 to 0.010 and -0.004; 95% CI, -0.020 to 0.012, respectively). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: -0.008; 95% CI, -0.058 to 0.042; IVAsian: 0.001; 95% CI, -0.036 to 0.036).
Conclusion: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.抄録：英語フィールド
Author：*Fujii R, Hishida A, Nishiyama T, Nakatochi M, Matsuo K, Ito H, Nishida Y, Shimanoe C, Nakamura Y, Turin TC, Suzuki S, Watanabe M, Ibusuki R, Takezaki T, Mikami H, Nakamura Y, Ikezaki H, Murata M, Kuriki K, Kuriyama N, Matsui D, Arisawa K, Katsuura-Kamano S, Tsukamoto M, Tamura T, Kubo Y, Kondo T, Momozawa Y, Kubo M, Takeuchi K, Wakai KTitle：Assessing the Relationship Between High-sensitivity C-reactive Protein and Kidney Function Employing Mendelian Randomization in the Japanese Community-based J-MICC StudyAnnouncement information:J Epidemiol Vol: 32 Issue: 11 Page: 483-488Keyword：Mendelian randomization study; eGFR; genetic epidemiology; hs-CRP; inflammationAn abstract：Background: Inflammation is thought to be a risk factor for kidney disease. However, whether inflammatory status is either a cause or an outcome of chronic kidney disease remains controversial. 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), 0.000; 95% confidence interval [CI], -0.019 to 0.020 and -0.003; 95% CI, -0.019 to 0.014, respectively). For IVAsian, we found similar results using the IVW and the WM methods (estimate, 0.005; 95% CI, -0.020 to 0.010 and -0.004; 95% CI, -0.020 to 0.012, respectively). The MR-Egger method also showed no causal relationships between hs-CRP and eGFR (IVCRP: -0.008; 95% CI, -0.058 to 0.042; IVAsian: 0.001; 95% CI, -0.036 to 0.036).
Conclusion: Our two-sample MR analyses with different IVs did not support a causal effect of hs-CRP on eGFR.