<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(12)</volume><submitter>Zhao Y</submitter><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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&lt;sup>14&lt;/sup>, P for MR-Egger =0.024) and cardiomyopathy (OR: 5.35×10&lt;sup>13&lt;/sup>; SE=±7.18×10&lt;sup>6&lt;/sup>, P for IVW=0.045 for finn-a-I9_CARDMYO, and OR: 3.60×10&lt;sup>25&lt;/sup>; SE=±3.26×10&lt;sup>12&lt;/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).&lt;h4>Conclusions&lt;/h4>We confirmed KSD may trigger causal pathological processes including coronary atherosclerosis and cardiomyopathy. Furthermore, hypertension may causally affect KSD.</pubmed_abstract><journal>Translational andrology and urology</journal><pagination>4344-4352</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8749067</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Kidney stone disease and cardiovascular events: a study on bidirectional causality based on mendelian randomization.</pubmed_title><pmcid>PMC8749067</pmcid><pubmed_authors>Wang M</pubmed_authors><pubmed_authors>Zhou M</pubmed_authors><pubmed_authors>Fan Y</pubmed_authors><pubmed_authors>Yu C</pubmed_authors><pubmed_authors>Du D</pubmed_authors><pubmed_authors>Jiang D</pubmed_authors><pubmed_authors>Chen S</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors><pubmed_authors>Tu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Kidney stone disease and cardiovascular events: a study on bidirectional causality based on mendelian randomization.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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&lt;sup>14&lt;/sup>, P for MR-Egger =0.024) and cardiomyopathy (OR: 5.35×10&lt;sup>13&lt;/sup>; SE=±7.18×10&lt;sup>6&lt;/sup>, P for IVW=0.045 for finn-a-I9_CARDMYO, and OR: 3.60×10&lt;sup>25&lt;/sup>; SE=±3.26×10&lt;sup>12&lt;/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).&lt;h4>Conclusions&lt;/h4>We confirmed KSD may trigger causal pathological processes including coronary atherosclerosis and cardiomyopathy. Furthermore, hypertension may causally affect KSD.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2025-04-04T19:40:48.875Z</modification><creation>2025-04-04T19:40:48.875Z</creation></dates><accession>S-EPMC8749067</accession><cross_references><pubmed>35070816</pubmed><doi>10.21037/tau-21-899</doi></cross_references></HashMap>