Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/38322
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dc.contributor.authorHapca, Simonaen_UK
dc.contributor.authorYang, Qinboen_UK
dc.contributor.authorLi, Sheyuen_UK
dc.contributor.authorMcGurnaghan, Stuart Jen_UK
dc.contributor.authorBlackbourn, Luke A Ken_UK
dc.contributor.authorPearson, Ewan Ren_UK
dc.contributor.authorColhoun, Helen Men_UK
dc.contributor.authorBell, Samiraen_UK
dc.date.accessioned2026-09-18T00:26:39Z-
dc.date.available2026-09-18T00:26:39Z-
dc.date.issued2026-09en_UK
dc.identifier.urihttp://hdl.handle.net/1893/38322-
dc.description.abstractIntroduction Variability in estimated glomerular filtration rate (eGFR) has been associated with increased risks of mortality and chronic kidney disease (CKD) progression in people with type 2 diabetes mellitus (T2DM) and impaired kidney function. However, its significance in individuals with preserved kidney function remains unclear. Methods In this nationwide retrospective population-based study of individuals with T2DM, eGFR variability was calculated by fitting a linear regression model to longitudinal data to estimate both the individual eGFR slope over the 5-year period as well as the variability in model residuals provided by the SD of the model residuals using longitudinal serum creatinine (SCr) measurements obtained during the first 5 years after diagnosis. Cox proportional hazards models were then applied to assess the association between eGFR variability and progression to stage G3b CKD among participants with preserved kidney function. Results This study included 98,322 participants who had an eGFR > 60 ml/min per 1.73 m2 at diagnosis, remained alive with an eGFR > 60 ml/min per 1.73 m2 5 years after diagnosis, and were subsequently followed for a mean of 5.1 years. Greater eGFR variability was associated with an increased risk of progression to stage G3b CKD- hazard ratios (HRs) for the second, third, and fourth quartiles of variability versus the first quartile were 1.56 (95% confidence interval [CI]: 1.38-1.75), 1.85 (95% CI: 1.65-2.08), and 2.56 (95% CI: 2.29-2.86), respectively. This association persisted after adjustment for multiple variables-HR: 1.57; 95% CI: 1.40-1.77 for the fourth quartiles of variability versus the first quartile. Conclusion eGFR variability in the absence of acute kidney injury (AKI) is associated with CKD progression in individuals with T2DM and preserved kidney function.en_UK
dc.language.isoenen_UK
dc.publisherElsevier BVen_UK
dc.relationHapca S, Yang Q, Li S, McGurnaghan SJ, Blackbourn LAK, Pearson ER, Colhoun HM & Bell S (2026) The Impact of Non-AKI eGFR Variability on CKD Progression in Individuals With Type 2 Diabetes and Preserved Kidney Function. <i>Kidney International Reports</i>, 11 (9), p. 106667. https://doi.org/10.1016/j.ekir.2026.106667en_UK
dc.rightsThis is an open access article distributed under the terms of the Creative Commons CC-BY license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. You are not required to obtain permission to reuse this article.en_UK
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_UK
dc.subjectGFR variabilityen_UK
dc.subjectchronic kidney diseaseen_UK
dc.subjectdiabetesen_UK
dc.titleThe Impact of Non-AKI eGFR Variability on CKD Progression in Individuals With Type 2 Diabetes and Preserved Kidney Functionen_UK
dc.typeJournal Articleen_UK
dc.identifier.doi10.1016/j.ekir.2026.106667en_UK
dc.identifier.pmid42490958en_UK
dc.citation.jtitleKidney Internationalen_UK
dc.citation.issn1523-1755en_UK
dc.citation.issn0085-2538en_UK
dc.citation.volume11en_UK
dc.citation.issue9en_UK
dc.citation.spage106667en_UK
dc.citation.publicationstatusPublisheden_UK
dc.citation.peerreviewedRefereeden_UK
dc.type.statusVoR - Version of Recorden_UK
dc.contributor.funderUniversity of Stirlingen_UK
dc.contributor.funderUniversity of Dundeeen_UK
dc.author.emailsimona.hapca@stir.ac.uken_UK
dc.citation.date18/06/2026en_UK
dc.contributor.affiliationComputing Scienceen_UK
dc.contributor.affiliationSichuan Universityen_UK
dc.contributor.affiliationSichuan Universityen_UK
dc.contributor.affiliationUniversity of Edinburghen_UK
dc.contributor.affiliationUniversity of Edinburghen_UK
dc.contributor.affiliationUniversity of Dundeeen_UK
dc.contributor.affiliationUniversity of Edinburghen_UK
dc.contributor.affiliationUniversity of Dundeeen_UK
dc.identifier.isiWOS:001827283000001en_UK
dc.identifier.scopusid105044908261en_UK
dc.identifier.wtid2285347en_UK
dc.contributor.orcid0000-0003-3148-9657en_UK
dc.date.accepted2026-06-08en_UK
dcterms.dateAccepted2026-06-08en_UK
dc.date.filedepositdate2026-08-10en_UK
rioxxterms.apcnot requireden_UK
rioxxterms.versionVoRen_UK
local.rioxx.authorHapca, Simona|0000-0003-3148-9657en_UK
local.rioxx.authorYang, Qinbo|en_UK
local.rioxx.authorLi, Sheyu|en_UK
local.rioxx.authorMcGurnaghan, Stuart J|en_UK
local.rioxx.authorBlackbourn, Luke A K|en_UK
local.rioxx.authorPearson, Ewan R|en_UK
local.rioxx.authorColhoun, Helen M|en_UK
local.rioxx.authorBell, Samira|en_UK
local.rioxx.projectProject ID unknown|University of Dundee|http://dx.doi.org/10.13039/100008890en_UK
local.rioxx.projectProject ID unknown|University of Stirling|en_UK
local.rioxx.freetoreaddate2026-09-14en_UK
local.rioxx.licencehttp://creativecommons.org/licenses/by/4.0/|2026-09-14|en_UK
local.rioxx.filenameSHapca_Kidney_International_Reports_2026.pdfen_UK
local.rioxx.filecount1en_UK
local.rioxx.source1523-1755en_UK
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