Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17178
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dc.contributor.authorBarr, Elizabeth L M-
dc.contributor.authorBarzi, Federica-
dc.contributor.authorHughes, Jaquelyne T-
dc.contributor.authorJerums, George-
dc.contributor.authorHoy, Wendy E-
dc.contributor.authorO'Dea, Kerin-
dc.contributor.authorJones, Graham-
dc.contributor.authorLawton, Paul D-
dc.contributor.authorBrown, Alex D H-
dc.contributor.authorThomas, Mark-
dc.contributor.authorEkinci, Elif I-
dc.contributor.authorSinha, Ashim-
dc.contributor.authorCass, Alan-
dc.contributor.authorMacIsaac, Richard J-
dc.contributor.authorMaple-Brown, Louise J-
dc.date2018-01-24-
dc.date.accessioned2018-02-22T04:02:21Z-
dc.date.available2018-02-22T04:02:21Z-
dc.date.issued2018-04-
dc.identifier.citationDiabetes Care 2018; 41(4): 739-747en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17178-
dc.description.abstractTo examine the association between soluble tumor necrosis factor receptor 1 (sTNFR1) levels and kidney disease progression in Indigenous Australians at high risk of kidney disease. This longitudinal observational study examined participants aged ≥18 years recruited from >20 sites across diabetes and/or kidney function strata. Baseline measures included sTNFR1, serum creatinine, urine albumin-to-creatinine ratio (uACR), HbA1c, C-reactive protein (CRP), waist-to-hip ratio, systolic blood pressure, and medical history. Linear regression was used to estimate annual change in estimated glomerular filtration rate (eGFR) for increasing sTNFR1, and Cox proportional hazards were used to estimate the hazard ratio (HR) and 95% CI for developing a combined renal outcome (first of a ≥30% decline in eGFR with a follow-up eGFR <60 mL/min/1.73 m2, progression to renal replacement therapy, or renal death) for increasing sTNFR1. Over a median of 3 years, participants with diabetes (n= 194) in the highest compared with the lowest quartile of sTNFR1 experienced significantly greater eGFR decline (-4.22 mL/min/1.73 m2/year [95% CI -7.06 to -1.38];P= 0.004), independent of baseline age, sex, eGFR, and uACR. The adjusted HR (95% CI) for participants with diabetes per doubling of sTNFR1 for the combined renal outcome (n= 32) was 3.8 (1.1-12.8;P= 0.03). No association between sTNFR1 and either renal outcome was observed for those without diabetes (n= 259). sTNFR1 is associated with greater kidney disease progression independent of albuminuria and eGFR in Indigenous Australians with diabetes. Further research is required to assess whether TNFR1 operates independently of other metabolic factors associated with kidney disease progression.en_US
dc.language.isoeng-
dc.titleHigh Baseline Levels of Tumor Necrosis Factor Receptor 1 Are Associated With Progression of Kidney Disease in Indigenous Australians With Diabetes: The eGFR Follow-up Study.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleDiabetes Careen_US
dc.identifier.affiliationMenzies School of Health Research, Darwin, Northern Territory, Australiaen_US
dc.identifier.affiliationBaker Heart and Diabetes Institute, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationRoyal Darwin Hospital, Darwin, Northern Territory, Australiaen_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationThe University of Queensland, Brisbane, Queensland, Australiaen_US
dc.identifier.affiliationNutrition and Population Health, University of South Australia, Adelaide, South Australia, Australiaen_US
dc.identifier.affiliationSt Vincent's Hospital, SydPath, Sydney, New South Wales, Australiaen_US
dc.identifier.affiliationDepartment of Medicine, University of New South Wales, Sydney, New South Wales, Australiaen_US
dc.identifier.affiliationAboriginal Health, Sansom Institute Health Research Operations, University of South Australia, Adelaide, South Australia, Australiaen_US
dc.identifier.affiliationIndigenous Health, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australiaen_US
dc.identifier.affiliationRoyal Perth Hospital, Perth, Western Australia, Australiaen_US
dc.identifier.affiliationDiabetes and Endocrinology, Cairns Base Hospital, Cairns, Queensland, Australiaen_US
dc.identifier.affiliationDepartment of Endocrinology and Diabetes, St Vincent's Hospital Melbourne, Melbourne, Victoria, Australiaen_US
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/29367427en_US
dc.identifier.doi10.2337/dc17-1919en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0003-4284-1716en_US
dc.identifier.orcid0000-0003-2372-395Xen_US
dc.identifier.orcid0000-0001-8058-6977en_US
dc.type.austinJournal Article-
local.name.researcherEkinci, Elif I
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
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