{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T04:14:30Z","timestamp":1789100070530,"version":"build-2803163510"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","funder":[{"DOI":"10.13039\/100000062","name":"NIDDK","doi-asserted-by":"crossref","award":["U01 DK094176 and U01 DK094157"],"award-info":[{"award-number":["U01 DK094176 and U01 DK094157"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000053","name":"National Eye Institute","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100000053","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"crossref"}]},{"name":"General Clinical Research Centers Program"},{"name":"Clinical Translational Science Center Program"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["CJASN"],"published-print":{"date-parts":[[2026,9]]},"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>Previous research has identified polygenic risk scores that are associated with low eGFR and albuminuria in the general population.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>We observed that these eGFR and albuminuria polygenic risk scores were associated with eGFR and albuminuria, respectively, in type 1 diabetes.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Associations were independent of glycemic control and suggest shared genetic kidney risk factors between type 1 diabetes and the general population.<\/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>Genetic risk factors underlying kidney disease in type 1 diabetes (T1D) remain poorly understood. We examined whether previously established polygenic risk scores (PRS) for eGFR and albuminuria are associated with these measures in adults with T1D in the Diabetes Control and Complications Trial (DCCT)\/Epidemiology of Diabetes Interventions and Complications study.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We applied eGFR and albuminuria PRS derived in general population cohorts to 1304 DCCT\/Epidemiology of Diabetes Interventions and Complications participants with genome-wide genotyping. We tested PRS associations with eGFR and urine albumin excretion rate (AER) as well as incident eGFR &lt;60 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      , AER \u226530 mg\/24 h, and AER \u2265300 mg\/24 h. For consistency, PRS values were linearly transformed so higher scores corresponded to higher eGFR and AER. We also examined associations of kidney outcomes with rs55703767 in\n                      <jats:italic toggle=\"yes\">COL4A3<\/jats:italic>\n                      , which has previously been associated with CKD in T1D.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At DCCT baseline, participants had a mean age of 27 years; 53% were male. 49% of participants were randomized to intensive versus conventional glucose-lowering therapy. Participants were followed for median of (first\u2013third quartiles) 35 (33\u201337) years. The eGFR PRS was significantly associated with continuous eGFR (per one SD higher PRS 2.72 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      higher [95% confidence interval (CI), 2.05 to 3.40]) and incident eGFR &lt;60 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      (hazard ratio [HR]=0.82 [95% CI, 0.73 to 0.92]), but not consistently with albuminuria. There was no association with quantitative AER (2.42 mg\/24 h [95% CI, \u22121.86 to 6.89]) or sustained AER \u226530 mg\/24 h (HR=1.03; [95% CI, 0.94 to 1.14]). The albuminuria PRS was significantly associated with incident AER \u226530 mg\/24 h (HR=1.12 [95% CI, 1.02 to 1.22]) but not continuous eGFR (0.49 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      higher [95% CI, \u22120.23 to 1.21]) or incident eGFR &lt;60 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      (HR=0.96 [95% CI, 0.85 to 1.08]). Associations were similar in analyses stratified by DCCT treatment group assignment. rs55703767 was associated with lower incident macroalbuminuria in the overall cohort (HR=0.77 per minor allele [95% CI, 0.59 to 0.99]), and upon stratification by DCCT treatment group assignment, only within the conventional and not intensive glucose-lowering therapy group.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>PRS associated with eGFR and albuminuria in the general population were associated with corresponding measures in adults with T1D. The results suggest shared genetic risk factors for kidney disease between T1D and the general population but different genetic risk factors for albuminuria and eGFR in T1D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical Trials Registration Numbers:<\/jats:title>\n                    <jats:p>NCT00360893, NCT00360815.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2215\/cjn.0000001111","type":"journal-article","created":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T16:09:41Z","timestamp":1782749381000},"page":"1554-1564","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Genetic Risk Factors for Kidney Function in Individuals with Type 1 Diabetes"],"prefix":"10.2215","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9162-7428","authenticated-orcid":false,"given":"Christine P.","family":"Limonte","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington"},{"name":"Kidney Research Institute, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0633-8996","authenticated-orcid":false,"given":"Xiaoyu","family":"Gao","sequence":"additional","affiliation":[{"name":"Biostatistics Center, The George Washington University, Rockville, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4902-8587","authenticated-orcid":false,"given":"Delnaz","family":"Roshandel","sequence":"additional","affiliation":[{"name":"Program in Genetics and Genome Biology, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4944-7968","authenticated-orcid":false,"given":"Ionut","family":"Bebu","sequence":"additional","affiliation":[{"name":"Biostatistics Center, The George Washington University, Rockville, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2781-3824","authenticated-orcid":false,"given":"Amy B.","family":"Karger","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gayle M.","family":"Lorenzi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of California San Diego, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1571-7592","authenticated-orcid":false,"given":"Ian H.","family":"de Boer","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington"},{"name":"Kidney Research Institute, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5885-0046","authenticated-orcid":false,"given":"Bruce A.","family":"Perkins","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, University of Toronto and University Health Network, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9169-118X","authenticated-orcid":false,"given":"Andrew D.","family":"Paterson","sequence":"additional","affiliation":[{"name":"Program in Genetics and Genome Biology, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada"},{"name":"Divisions of Epidemiology and Biostatistics, Dalla Lana School of Public 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