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CH, defined as mosaic chromosome abnormalities (mCA) and\/or driver mutations was identified in 5449 (2.9%) eligible UK Biobank participants (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u2009190,487 median age\u2009=\u200958 years). CH was negatively associated with glomerular filtration rate estimated from cystatin-C (eGFR.cys;\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2009=\u2009\u22120.75,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20092.37\u2009\u00d7\u200910\n                    <jats:sup>\u20134<\/jats:sup>\n                    ), but not with eGFR estimated from creatinine, and was specifically associated with CKD defined by eGFR.cys\u2009&lt;\u200960 (OR\u2009=\u20091.02,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20098.44\u2009\u00d7\u200910\n                    <jats:sup>\u20138<\/jats:sup>\n                    ). In participants without prevalent myeloid neoplasms, eGFR.cys was associated with myeloid mCA (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u2009148,\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2009=\u2009\u22123.36,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.01) and somatic driver mutations (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20093241,\n                    <jats:italic>\u03b2<\/jats:italic>\n                    \u2009=\u2009\u22121.08,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20096.25\u2009\u00d7\u200910\n                    <jats:sup>\u20135<\/jats:sup>\n                    ) associated with myeloid neoplasia (myeloid CH), specifically mutations in\n                    <jats:italic>CBL<\/jats:italic>\n                    ,\n                    <jats:italic>TET2<\/jats:italic>\n                    ,\n                    <jats:italic>JAK2<\/jats:italic>\n                    ,\n                    <jats:italic>PPM1D<\/jats:italic>\n                    and\n                    <jats:italic>GNB1<\/jats:italic>\n                    but not\n                    <jats:italic>DNMT3A<\/jats:italic>\n                    or\n                    <jats:italic>ASXL1<\/jats:italic>\n                    . In participants with no history of cardiovascular disease or myeloid neoplasms, myeloid CH increased the risk of adverse outcomes in CKD (HR\u2009=\u20091.6,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.002) compared to those without myeloid CH. Mendelian randomisation analysis provided suggestive evidence for a causal relationship between CH and CKD (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.03). We conclude that CH, and specifically myeloid CH, is associated with CKD defined by eGFR.cys. Myeloid CH promotes adverse outcomes in CKD, highlighting the importance of the interaction between intrinsic and extrinsic factors to define the health risk associated with CH.\n                  <\/jats:p>","DOI":"10.1038\/s41375-021-01382-3","type":"journal-article","created":{"date-parts":[[2021,8,19]],"date-time":"2021-08-19T15:04:41Z","timestamp":1629385481000},"page":"507-515","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":91,"title":["Clonal myelopoiesis promotes adverse outcomes in chronic kidney disease"],"prefix":"10.1038","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0164-7773","authenticated-orcid":false,"given":"Ahmed A. 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