{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:55:22Z","timestamp":1779238522547,"version":"3.51.4"},"reference-count":40,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,1,27]],"date-time":"2013-01-27T00:00:00Z","timestamp":1359244800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Transplantation"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Chronic allograft dysfunction (<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>) is a common outcome in kidney transplants, but its pathogenesis is unclear. We investigated the<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>phenotype and single\u2010nucleotide polymorphisms (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s) associated with<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>This prospective study enrolled 2336 transplants from seven transplant centers in North America.<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>was defined as a &gt;25% rise in serum creatinine relative to a three\u2010month post\u2010transplant baseline, requiring a kidney biopsy. We genotyped 2724<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s in the initial 979 transplants, which form the test cohort.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>occurred 11.2 times per 100 person\u2010years at a median of 509\u00a0\u00b1\u00a0387\u00a0days from the three\u2010month baseline.<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>was independently associated with death\u2010censored, allograft failure, in an adjusted analysis [<jats:styled-content style=\"fixed-case\">HR<\/jats:styled-content>=20.6 (11.8\u201335.8, p\u00a0&lt;\u00a00.001)]. Among 366 transplant recipients with<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>, 91% had inflammation on biopsy scores. 94 (26%) had inflammatory changes consistent with a diagnosis of concomitant acute rejection.<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s in<jats:italic><jats:styled-content style=\"fixed-case\">FM<\/jats:styled-content>06<\/jats:italic>and<jats:italic><jats:styled-content style=\"fixed-case\">FM<\/jats:styled-content>03,<\/jats:italic>potential drug metabolism genes, were associated with<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>, after accounting for multiple testing.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>phenotype with concomitant inflammation is associated with increased risk of allograft failure.<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s associated with<jats:styled-content style=\"fixed-case\">CGD<\/jats:styled-content>in novel drug metabolism and transport genes, will be validated in subsequent transplants.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ctr.12074","type":"journal-article","created":{"date-parts":[[2013,1,28]],"date-time":"2013-01-28T03:22:04Z","timestamp":1359343324000},"page":"348-358","source":"Crossref","is-referenced-by-count":15,"title":["Inflammation in the setting of chronic allograft dysfunction post\u2010kidney transplant: phenotype and genotype"],"prefix":"10.1111","volume":"27","author":[{"given":"Ajay K.","family":"Israni","sequence":"first","affiliation":[{"name":"Nephrology Division Department of Medicine Hennepin County Medical Center, University of Minnesota"},{"name":"Department of Epidemiology and Community Health University of Minnesota Minneapolis MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert","family":"Leduc","sequence":"additional","affiliation":[{"name":"Division 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USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arthur J.","family":"Matas","sequence":"additional","affiliation":[{"name":"Department of Surgery University of Minnesota Minneapolis MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William S.","family":"Oetting","sequence":"additional","affiliation":[{"name":"Department of Experimental and Clinical Pharmacology University of Minnesota Minneapolis MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"name":"The DeKAF Genomics 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