{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T01:18:25Z","timestamp":1784078305344,"version":"3.55.0"},"reference-count":45,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2024,8,21]],"date-time":"2024-08-21T00:00:00Z","timestamp":1724198400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Kidney function can be impaired in patients with inflammatory bowel diseases (IBD), including Crohn's diseases (CD) and ulcerative colitis (UC). However, the causal relationship between IBD and chronic kidney diseases (CKD) remains unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We determined the causal association between IBD and CKD by performing two\u2010sample bidirectional mendelian randomization (MR) analyses. Independent genetic variants were selected as instrumental variables (IVs) of the exposure from open\u2010access genome\u2010wide association studies (GWAS) among European ancestry. IVs\u2013outcome estimates were extracted from three separate GWAS for IBD and two for CKD, respectively. Inverse\u2010variance\u2010weighted model was used as the primary MR method. The pleiotropic effect and heterogeneity were evaluated. For either direction, analyses were performed per outcome database and were subsequently meta\u2010analysed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Genetically predicted IBD was associated with higher risk of CKD (OR: 1.045, 95% CI: 1.016\u20131.073, <jats:italic>P<\/jats:italic>\u2009=\u20090.002) by including 42\u2009344 IBD cases and 229\u2009164 controls. Further analyses showed genetic liability to CD increased the risk of CKD (OR: 1.057, 95% CI: 1.027\u20131.087, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) whereas UC did not (OR: 0.999, 95% CI:0.969\u20131.031, <jats:italic>p<\/jats:italic>\u2009=\u20090.970). In contrast, genetically predicted CKD was not associated with IBD (OR: 1.010, 95% CI: 0.965\u20131.056, <jats:italic>p<\/jats:italic>\u2009=\u20090.676), UC (OR: 1.011, 95% CI: 0.948\u20131.078, <jats:italic>p<\/jats:italic>\u2009=\u20090.746) and CD (OR: 1.024; 95% CI: 0.963\u20131.089, <jats:italic>p<\/jats:italic>\u2009=\u20090.447).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We concluded that CD, but not UC, can increase the risk of CKD causally. CD, but not UC, can increase the risk of chronic kidney disease causally. These findings enhance our understanding of the differential impact of IBD subtypes on CKD. It may be necessary to monitor kidney function regularly in patients with CD.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nep.14371","type":"journal-article","created":{"date-parts":[[2024,8,22]],"date-time":"2024-08-22T03:15:26Z","timestamp":1724296526000},"page":"738-747","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Assessment of the causal relationship between inflammatory bowel diseases and chronic kidney diseases: A two\u2010sample bidirectional mendelian randomization study among European population"],"prefix":"10.1111","volume":"29","author":[{"given":"Xingxing","family":"Li","sequence":"first","affiliation":[{"name":"West China School of Public Health and West China Fourth Hospital Sichuan University  Chengdu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiaoyue","family":"Ge","sequence":"additional","affiliation":[{"name":"West China School of Public Health and West China Fourth 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