{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10(12)"],"submitter":["Zhao Y"],"pubmed_abstract":["<h4>Background</h4>Kidney stone disease (KSD) has been reported to be associated with several cardiovascular diseases. However, the causality between the conditions remains unknown. In the study, we performed a study on bidirectional causality by two-sample Mendelian randomization (MR) to investigate the causality between KSD and cardiovascular diseases including coronary atherosclerosis, hypertension, and cardiomyopathy.<h4>Methods</h4>In the recent study, we performed a bidirectional two-sample MR study using available genome-wide association summary data from the online database MRBASE. We identified genetic variants associated with KSD in one European population from UK Biobank (version 2, n=462,933). Two phenotypes of samples were chosen from the population to define our genetic instrumental variables: (I) samples with the phenotype of kidney stone/ureter stone/bladder stone (ukb-b-8297), and (II) samples with the phenotype of kidney stone surgery/lithotripsy (ukb-b-13537). For cardiovascular diseases, we picked up another independent European population from FinnGen Biobank (n=93,421). We selected the exposure and outcome SNPs and then performed the two-sample MR using R package.<h4>Results</h4>After bidirectional causality by two-sample MR, we verified that genetic predisposition to KSD could increase the risk of coronary atherosclerosis (OR: 4.45×1037; SE=±7.80×10<sup>14</sup>, P for MR-Egger =0.024) and cardiomyopathy (OR: 5.35×10<sup>13</sup>; SE=±7.18×10<sup>6</sup>, P for IVW=0.045 for finn-a-I9_CARDMYO, and OR: 3.60×10<sup>25</sup>; SE=±3.26×10<sup>12</sup>, P for IVW=0.041 for finn-a-I9_CARDMYOOTH) when we used ukb-b-13537 as exposure group. Furthermore, hypertension could increase the risk of KSD (OR: 1.001; SE=±1.00, P for IVW=0.003) when we used ukb-b-8297 as exposure group, without detected pleiotropy bias (P>0.05).<h4>Conclusions</h4>We confirmed KSD may trigger causal pathological processes including coronary atherosclerosis and cardiomyopathy. Furthermore, hypertension may causally affect KSD."],"journal":["Translational andrology and urology"],"pagination":["4344-4352"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8749067"],"repository":["biostudies-literature"],"pubmed_title":["Kidney stone disease and cardiovascular events: a study on bidirectional causality based on mendelian randomization."],"pmcid":["PMC8749067"],"pubmed_authors":["Wang M","Zhou M","Fan Y","Yu C","Du D","Jiang D","Chen S","Zhao Y","Tu X"],"additional_accession":[]},"is_claimable":false,"name":"Kidney stone disease and cardiovascular events: a study on bidirectional causality based on mendelian randomization.","description":"<h4>Background</h4>Kidney stone disease (KSD) has been reported to be associated with several cardiovascular diseases. However, the causality between the conditions remains unknown. In the study, we performed a study on bidirectional causality by two-sample Mendelian randomization (MR) to investigate the causality between KSD and cardiovascular diseases including coronary atherosclerosis, hypertension, and cardiomyopathy.<h4>Methods</h4>In the recent study, we performed a bidirectional two-sample MR study using available genome-wide association summary data from the online database MRBASE. We identified genetic variants associated with KSD in one European population from UK Biobank (version 2, n=462,933). Two phenotypes of samples were chosen from the population to define our genetic instrumental variables: (I) samples with the phenotype of kidney stone/ureter stone/bladder stone (ukb-b-8297), and (II) samples with the phenotype of kidney stone surgery/lithotripsy (ukb-b-13537). For cardiovascular diseases, we picked up another independent European population from FinnGen Biobank (n=93,421). We selected the exposure and outcome SNPs and then performed the two-sample MR using R package.<h4>Results</h4>After bidirectional causality by two-sample MR, we verified that genetic predisposition to KSD could increase the risk of coronary atherosclerosis (OR: 4.45×1037; SE=±7.80×10<sup>14</sup>, P for MR-Egger =0.024) and cardiomyopathy (OR: 5.35×10<sup>13</sup>; SE=±7.18×10<sup>6</sup>, P for IVW=0.045 for finn-a-I9_CARDMYO, and OR: 3.60×10<sup>25</sup>; SE=±3.26×10<sup>12</sup>, P for IVW=0.041 for finn-a-I9_CARDMYOOTH) when we used ukb-b-13537 as exposure group. Furthermore, hypertension could increase the risk of KSD (OR: 1.001; SE=±1.00, P for IVW=0.003) when we used ukb-b-8297 as exposure group, without detected pleiotropy bias (P>0.05).<h4>Conclusions</h4>We confirmed KSD may trigger causal pathological processes including coronary atherosclerosis and cardiomyopathy. Furthermore, hypertension may causally affect KSD.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2025-04-04T19:40:48.875Z","creation":"2025-04-04T19:40:48.875Z"},"accession":"S-EPMC8749067","cross_references":{"pubmed":["35070816"],"doi":["10.21037/tau-21-899"]}}