{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T04:32:05Z","timestamp":1786422725573,"version":"build-2736575974"},"reference-count":52,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["R01DK125782"],"award-info":[{"award-number":["R01DK125782"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01DK132155"],"award-info":[{"award-number":["R01DK132155"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"crossref","award":["427810"],"award-info":[{"award-number":["427810"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["K99HG012956"],"award-info":[{"award-number":["K99HG012956"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            In patients with CKD, non-\n                            <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                            clonal hematopoiesis of indeterminate potential (CHIP) was associated with higher risk of cardiovascular events.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>There was no significant difference in the CHIP\u2013cardiovascular disease association based on baseline eGFR, diabetes status, or race.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            The protective effect of\n                            <jats:italic toggle=\"yes\">IL6R<\/jats:italic>\n                            p.Asp358Ala on non-\n                            <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                            CHIP cardiovascular risk was similar to the general population.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Patients with CKD are at higher risk of cardiovascular disease. Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with cardiovascular disease in the general population, with a causal role observed in animal models. In the general population, the effect of CHIP is greater for somatic mutations in predefined CHIP driver genes other than\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      (referred to as non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      CHIP). We sought to assess the prospective association between CHIP and cardiovascular events in patients with CKD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      CHIP was measured by high-depth targeted sequencing. The primary analysis tested the association of somatic mutations in non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      CHIP driver genes with a composite cardiovascular disease end point of myocardial infarction, stroke, congestive heart failure, and peripheral artery disease in 5043 patients with CKD in four prospective cohorts. Sensitivity analyses examined the effect of CHIP subtypes, race, baseline comorbidities,\n                      <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                      risk alleles, and\n                      <jats:italic toggle=\"yes\">IL6R<\/jats:italic>\n                      p.Asp358Ala genotype.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At baseline, patients had a mean age of 66\u00b112 years and eGFR of 43\u00b118 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      . CHIP was present in 24% of patients, with 13% of all patients carrying acquired non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      mutations. Non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      CHIP was associated with a 36% higher risk of the composite cardiovascular end point (95% confidence interval [CI], 6% to 76%). Among composite components, non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      CHIP was associated with a higher risk of stroke (hazard ratio, 1.65; 95% CI, 1.10 to 2.47). Baseline eGFR, diabetes status, or race did not alter the association of non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      CHIP with cardiovascular risk. Those without genetically reduced IL-6 signaling (noncarriers of\n                      <jats:italic toggle=\"yes\">IL6R<\/jats:italic>\n                      p.Asp358Ala) had worse disease (hazard ratio, 1.46; 95% CI, 1.17 to 1.83;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      <jats:sub>subgroup difference<\/jats:sub>\n                      = 0.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      In patients with CKD, non-\n                      <jats:italic toggle=\"yes\">DNMT3A<\/jats:italic>\n                      CHIP was associated with cardiovascular disease with an effect size similar to that reported in the general population.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.0000000671","type":"journal-article","created":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T12:06:46Z","timestamp":1744200406000},"page":"1775-1785","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":10,"title":["Association of Clonal Hematopoiesis of Indeterminate Potential with Cardiovascular Events in Patients with CKD"],"prefix":"10.1681","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3487-7233","authenticated-orcid":false,"given":"Yang","family":"Pan","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, College of Medicine, University of Illinois Chicago, Chicago, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-8466-7602","authenticated-orcid":false,"given":"Caitlyn","family":"Vlasschaert","sequence":"additional","affiliation":[{"name":"Department of Medicine, Queen's 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