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Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry
BACKGROUND: This study aimed to investigate a causal relationship between IBD and multiple kidney diseases using two-sample Mendelian randomization (MR) analyses. METHODS: We selected a group of single nucleotide polymorphisms (SNPs) specific to IBD as instrumental variables from a published genome-...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10521387/ https://www.ncbi.nlm.nih.gov/pubmed/37752523 http://dx.doi.org/10.1186/s12920-023-01644-2 |
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author | Lian, Xingji Wang, Yiqin Wang, Shuyi Peng, Xiaohui Wang, Yanhui Huang, Yuyu Chen, Wei |
author_facet | Lian, Xingji Wang, Yiqin Wang, Shuyi Peng, Xiaohui Wang, Yanhui Huang, Yuyu Chen, Wei |
author_sort | Lian, Xingji |
collection | PubMed |
description | BACKGROUND: This study aimed to investigate a causal relationship between IBD and multiple kidney diseases using two-sample Mendelian randomization (MR) analyses. METHODS: We selected a group of single nucleotide polymorphisms (SNPs) specific to IBD as instrumental variables from a published genome-wide association study (GWAS) with 86,640 individuals of European ancestry. Summary statistics for multiple kidney diseases were obtained from the publicly available GWAS. Genetic data from one GWAS involving 210 extensive T-cell traits was used to estimate the mediating effect on specific kidney disease. Inverse-variance weighted method were used to evaluate the MR estimates for primary analysis. RESULTS: Genetic predisposition to IBD was associated with higher risk of IgA nephropathy (IgAN) (OR, 1.78; 95% CI, 1.45–2.19), but not membranous nephropathy, diabetic nephropathy, glomerulonephritis, nephrotic syndrome, chronic kidney disease, and urolithiasis. CD4 expression on CD4 + T cell had a significant genetic association with the risk of IgAN (OR, 2.72; 95% CI, 1.10–6.72). Additionally, consistent results were also observed when IBD was subclassified as ulcerative colitis (OR, 1.38; 95% CI, 1.10–1.71) and Crohn’s disease (OR, 1.37; 95% CI, 1.12–1.68). MR-PRESSO and the MR-Egger intercept did not identify pleiotropic SNPs. CONCLUSIONS: This study provides genetic evidence supporting a positive casual association between IBD, including its subclassification as ulcerative colitis and Crohn’s disease, and the risk of IgAN. However, no casual association was found between IBD and other types of kidney diseases. Further exploration of IBD interventions as potential preventive measures for IgAN is warranted. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12920-023-01644-2. |
format | Online Article Text |
id | pubmed-10521387 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-105213872023-09-27 Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry Lian, Xingji Wang, Yiqin Wang, Shuyi Peng, Xiaohui Wang, Yanhui Huang, Yuyu Chen, Wei BMC Med Genomics Research BACKGROUND: This study aimed to investigate a causal relationship between IBD and multiple kidney diseases using two-sample Mendelian randomization (MR) analyses. METHODS: We selected a group of single nucleotide polymorphisms (SNPs) specific to IBD as instrumental variables from a published genome-wide association study (GWAS) with 86,640 individuals of European ancestry. Summary statistics for multiple kidney diseases were obtained from the publicly available GWAS. Genetic data from one GWAS involving 210 extensive T-cell traits was used to estimate the mediating effect on specific kidney disease. Inverse-variance weighted method were used to evaluate the MR estimates for primary analysis. RESULTS: Genetic predisposition to IBD was associated with higher risk of IgA nephropathy (IgAN) (OR, 1.78; 95% CI, 1.45–2.19), but not membranous nephropathy, diabetic nephropathy, glomerulonephritis, nephrotic syndrome, chronic kidney disease, and urolithiasis. CD4 expression on CD4 + T cell had a significant genetic association with the risk of IgAN (OR, 2.72; 95% CI, 1.10–6.72). Additionally, consistent results were also observed when IBD was subclassified as ulcerative colitis (OR, 1.38; 95% CI, 1.10–1.71) and Crohn’s disease (OR, 1.37; 95% CI, 1.12–1.68). MR-PRESSO and the MR-Egger intercept did not identify pleiotropic SNPs. CONCLUSIONS: This study provides genetic evidence supporting a positive casual association between IBD, including its subclassification as ulcerative colitis and Crohn’s disease, and the risk of IgAN. However, no casual association was found between IBD and other types of kidney diseases. Further exploration of IBD interventions as potential preventive measures for IgAN is warranted. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12920-023-01644-2. BioMed Central 2023-09-26 /pmc/articles/PMC10521387/ /pubmed/37752523 http://dx.doi.org/10.1186/s12920-023-01644-2 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Lian, Xingji Wang, Yiqin Wang, Shuyi Peng, Xiaohui Wang, Yanhui Huang, Yuyu Chen, Wei Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry |
title | Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry |
title_full | Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry |
title_fullStr | Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry |
title_full_unstemmed | Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry |
title_short | Does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of European ancestry |
title_sort | does inflammatory bowel disease promote kidney diseases: a mendelian randomization study with populations of european ancestry |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10521387/ https://www.ncbi.nlm.nih.gov/pubmed/37752523 http://dx.doi.org/10.1186/s12920-023-01644-2 |
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