{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T02:40:42Z","timestamp":1788316842762,"version":"build-2803163510"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"18","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2022,9,20]]},"abstract":"<jats:sec sec-type=\"background\" xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Differences in death rate and cardiovascular disease (CVD) between Black and White patients with chronic kidney disease is attributed to sociocultural factors, comorbidities, genetics, and inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      We examined the interaction of race, plasma IL\u20106 (interleukin\u20106), and\n                      <jats:italic>TMPRSS6<\/jats:italic>\n                      genotype as determinants of CVD and mortality in 3031 Chronic Renal Insufficiency Cohort study participants. The primary outcomes were all\u2010cause mortality and a composite of incident myocardial infarction, peripheral artery disease, stroke, and heart failure. During the median follow\u2010up of 10\u2009years, Black patients with chronic kidney disease experienced a significantly higher mortality (34% versus 26%) and CVD composite (41% versus 28%) compared with White patients. After adjustment,\n                      <jats:italic>TMPRSS6<\/jats:italic>\n                      genotype did not associate with the outcomes. The adjusted hazard ratio for mortality (4.11 [2.48\u20136.80],\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001) and CVD composite (2.52 [1.96\u20133.24],\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001) were higher for the highest versus lowest IL\u20106 quintile. The adjusted hazards for death per 1\u2010quintile increase in IL\u20106 in White and Black individuals were 1.53 (1.42\u20131.64) versus 1.29 (1.20\u20131.38) (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001), respectively. For CVD composite they were 1.61 (1.50\u20131.74) versus 1.30 (1.22\u20131.39) (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001), respectively. In Cox proportional hazard models that included IL\u20106, there was no longer a racial disparity for death (1.01 [0.87\u20131.16],\n                      <jats:italic>P<\/jats:italic>\n                      =0.92), but significant unexplained mediation remained for CVD (1.24 [1.07\u20131.43];\n                      <jats:italic>P<\/jats:italic>\n                      =0.004). Path models that included IL\u20106, diabetes, and urine albumin to creatinine ratio were able to identify variables responsible for racial disparity in mortality and CVD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Racial differences in mortality and CVD among patients with chronic kidney disease could be explained by good\u2010fitting path models that include selected mediator variables including diabetes and plasma IL\u20106.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.122.025627","type":"journal-article","created":{"date-parts":[[2022,9,14]],"date-time":"2022-09-14T05:55:44Z","timestamp":1663134944000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":10,"title":["Race, Interleukin\u20106,\n                    <i>TMPRSS6<\/i>\n                    Genotype, and Cardiovascular Disease in Patients With Chronic Kidney Disease"],"prefix":"10.1161","volume":"11","author":[{"given":"Ian R.","family":"Barrows","sequence":"first","affiliation":[{"name":"Division of Cardiology George Washington University School of Medicine Washington DC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1531-0303","authenticated-orcid":false,"given":"Matt","family":"Devalaraja","sequence":"additional","affiliation":[{"name":"Research &amp; Development Corvidia Therapeutics Waltham MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1273-0441","authenticated-orcid":false,"given":"Rahul","family":"Kakkar","sequence":"additional","affiliation":[{"name":"Research &amp; Development Corvidia Therapeutics Waltham 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S.","family":"Raj","sequence":"additional","affiliation":[{"name":"Division of Kidney Diseases and Hypertension, Department of Medicine The George Washington University School of Medicine and Health Sciences Washington DC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4900-653X","authenticated-orcid":false,"given":"Richard L.","family":"Amdur","sequence":"additional","affiliation":[{"name":"Department of Surgery The George Washington University School of Medicine and Health Sciences Washington DC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark L.","family":"Unruh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vallabh O.","family":"Shah","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Panduranga 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