{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T20:29:50Z","timestamp":1786480190203,"version":"build-2736575974"},"reference-count":18,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2025,10,6]],"date-time":"2025-10-06T00:00:00Z","timestamp":1759708800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["R01 DK071891"],"award-info":[{"award-number":["R01 DK071891"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["R01 DK071891"],"award-info":[{"award-number":["R01 DK071891"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2026,1]]},"abstract":"\n Key Points<\/jats:title>\n \n \n \n AKR1A1 depletion impairs tubule cell function.<\/jats:p>\n <\/jats:list-item>\n \n Higher serum AKR1A1 predicts slower eGFR decline rate.<\/jats:p>\n <\/jats:list-item>\n \n AKR1A1 could be a potential therapeutic target.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n Black Americans have disproportionately high rates of diabetic kidney disease (DKD). Identification of biomarkers predicting early DKD progression is essential to prescribe protective treatments before the development of irreversible histologic lesions and markedly reduced kidney function.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We tested whether\n AKR1A1<\/jats:italic>\n was a marker of early DKD progression through knock-out of\n AKR1A1<\/jats:italic>\n in a human kidney proximal tubule cell line and by measuring serum\n AKR1A1<\/jats:italic>\n concentrations in Black patients with type 2 diabetes (T2D).\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n AKR1A1<\/jats:italic>\n knockout cells had reduced cell viability, and the effect was aggravated by administering high-dose palmitate. In addition, higher serum\n AKR1A1<\/jats:italic>\n concentrations in Black patients with T2D and preserved kidney function predicted slower decline rate in eGFR over time.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n AKR1A1<\/jats:italic>\n seems to play a critical role in countering toxic effects of fatty acid metabolism and may prevent rapid decline of kidney function in Black patients with T2D.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.34067\/kid.0000000966","type":"journal-article","created":{"date-parts":[[2025,10,6]],"date-time":"2025-10-06T16:04:47Z","timestamp":1759766687000},"page":"131-138","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Serum AKR1A1 Levels Predict eGFR Decline Rate in Black Americans with Type 2 Diabetes"],"prefix":"10.34067","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7763-7793","authenticated-orcid":false,"given":"Lijun","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Internal Medicine \u2013 Section on Nephrology, Wake Forest University School of Medicine, Winston-Salem, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young A.","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine \u2013 Section on Nephrology, Wake Forest University School of Medicine, Winston-Salem, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DengFeng","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Biostatistics and Data Science, Wake Forest University School of Medicine, Winston-Salem, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9808-4518","authenticated-orcid":false,"given":"Moin A.","family":"Saleem","sequence":"additional","affiliation":[{"name":"Department of Renal Medicine, University of Bristol, Bristol, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0275-5530","authenticated-orcid":false,"given":"Barry I.","family":"Freedman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine \u2013 Section on Nephrology, Wake Forest University School of Medicine, Winston-Salem, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,10,6]]},"reference":[{"issue":"11","key":"B1-20260129","doi-asserted-by":"crossref","first-page":"2784","DOI":"10.1093\/ndt\/gfh470","article-title":"Remission to normoalbuminuria during multifactorial treatment preserves kidney function in patients with type 2 diabetes and microalbuminuria","volume":"19","author":"Gaede","year":"2004","journal-title":"Nephrol Dial Transplant."},{"issue":"8","key":"B2-20260129","doi-asserted-by":"crossref","first-page":"1347","DOI":"10.1007\/s00125-008-1051-7","article-title":"The kidney in diabetes: dynamic pathways of injury and repair. The Camillo Golgi Lecture 2007","volume":"51","author":"Fioretto","year":"2008","journal-title":"Diabetologia."},{"issue":"9","key":"B3-20260129","doi-asserted-by":"crossref","first-page":"1819","DOI":"10.1007\/s00125-016-4001-9","article-title":"Proteomics for prediction of disease progression and response to therapy in diabetic kidney disease","volume":"59","author":"Pena","year":"2016","journal-title":"Diabetologia."},{"issue":"7","key":"B4-20260129","doi-asserted-by":"crossref","first-page":"950","DOI":"10.1038\/s41588-022-01097-w","article-title":"Epigenomic and transcriptomic analyses define core cell types, genes and targetable mechanisms for kidney disease","volume":"54","author":"Liu","year":"2022","journal-title":"Nat Genet."},{"issue":"7","key":"B5-20260129","doi-asserted-by":"crossref","first-page":"1279","DOI":"10.1681\/ASN.0000000000000141","article-title":"Unbiased human kidney tissue proteomics identifies matrix metalloproteinase 7 as a kidney disease 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