biostudies-literatureMatias-Garcia PRNational Institute of Environmental Health SciencesBundesministerium für Bildung und ForschungJackson State UniversityNCATS NIH HHSNIA NIH HHSNIEHS NIH HHSNHLBI NIH HHSLudwig-Maximilians-Universität MünchenNational Institute on Minority Health and Health DisparitiesBundesministerium für Familie, Senioren, Frauen und JugendCooperative Studies Program/Epidemiology Research and Information Center of the U.S. Department of Veterans AffairsMinisterium für Wissenschaft, Forschung und Kunst Baden-WürttembergNIDDK NIH HHSUniversity of Mississippi Medical CenterTougaloo CollegeFoundation for the National Institutes of HealthNIMHD NIH HHSNational Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health and Human ServicesMichigan Department of Mental HealthNational Center for Advancing Translational Sciences, National Institutes of HealthHelmholtz Zentrum München121https://www.ebi.ac.uk/biostudies/studies/S-EPMC8170969biostudies-literatureUnknown13(1)<h4>Background</h4>The difference between an individual's chronological and DNA methylation predicted age (DNAmAge), termed DNAmAge acceleration (DNAmAA), can capture life-long environmental exposures and age-related physiological changes reflected in methylation status. Several studies have linked DNAmAA to morbidity and mortality, yet its relationship with kidney function has not been assessed. We evaluated the associations between seven DNAm aging and lifespan predictors (as well as GrimAge components) and five kidney traits (estimated glomerular filtration rate [eGFR], urine albumin-to-creatinine ratio [uACR], serum urate, microalbuminuria and chronic kidney disease [CKD]) in up to 9688 European, African American and Hispanic/Latino individuals from seven population-based studies.<h4>RClinical epigeneticsDNAm-based signatures of accelerated aging and mortality in blood are associated with low renal function.PMC8170969R01 ES025225R21-HL14038560442456 BAA23HHSN268201800014CHHSN268201800012CHHSN268201800012IHHSN268201800014IHHSN268201600003CHHSN268201800010IR01- MD012765HHSN268201600001CR01ES025225P30ES009089R01 DK117445R01-ES020836T32 HL129982P30ES009089, R01ES027747R01 MD012765HHSN268201800015IR01 ES020836R01-DK117445HHSN268201800011IHHSN268201800013IHHSN268201600002CKL2TR002490KL2 TR002490R21 HL140385HHSN268201600018CP30 ES009089HHSN268201600004CR01 ES027747U01 AG060908R01ES021733Wilson RYoung BPeters AShen JWinkelmann JWaldenberger MCoull BWard-Caviness CKCorrea ALin XBaccarelli AAJust ACLiu SEaton CWhitsel EANano JLange LMatias-Garcia PRLange EZheng YGieger CKunze SRaffield LMReiner AKoenig WColicino ESchwartz JFranceschini NHorvath SLu AHou LVokonas PAdamski JZhang YNwanaji-Enwerem JCSchottker BBostom ABrenner HGao XfalseDNAm-based signatures of accelerated aging and mortality in blood are associated with low renal function.<h4>Background</h4>The difference between an individual's chronological and DNA methylation predicted age (DNAmAge), termed DNAmAge acceleration (DNAmAA), can capture life-long environmental exposures and age-related physiological changes reflected in methylation status. Several studies have linked DNAmAA to morbidity and mortality, yet its relationship with kidney function has not been assessed. We evaluated the associations between seven DNAm aging and lifespan predictors (as well as GrimAge components) and five kidney traits (estimated glomerular filtration rate [eGFR], urine albumin-to-creatinine ratio [uACR], serum urate, microalbuminuria and chronic kidney disease [CKD]) in up to 9688 European, African American and Hispanic/Latino individuals from seven population-based studies.<h4>R2021-01-01T00:00:00Z2021 Jun2026-05-07T22:55:36.516Z2022-02-10T13:31:43.12ZS-EPMC81709693407845710.1186/s13148-021-01082-w