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|Title:||High 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.|
|Authors:||Barr, Elizabeth L M;Barzi, Federica;Hughes, Jaquelyne T;Jerums, George;Hoy, Wendy E;O'Dea, Kerin;Jones, Graham;Lawton, Paul D;Brown, Alex D H;Thomas, Mark;Ekinci, Elif I;Sinha, Ashim;Cass, Alan;MacIsaac, Richard J;Maple-Brown, Louise J|
|Affiliation:||Menzies School of Health Research, Darwin, Northern Territory, Australia|
Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia
Royal Darwin Hospital, Darwin, Northern Territory, Australia
Department of Endocrinology, Austin Health, Heidelberg, Victoria, Australia
Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia
The University of Queensland, Brisbane, Queensland, Australia..
Nutrition and Population Health, University of South Australia, Adelaide, South Australia, Australia..
St Vincent's Hospital, SydPath, Sydney, New South Wales, Australia
Department of Medicine, University of New South Wales, Sydney, New South Wales, Australia
Aboriginal Health, Sansom Institute Health Research Operations, University of South Australia, Adelaide, South Australia, Australia
Indigenous Health, South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
Royal Perth Hospital, Perth, Western Australia, Australia
Diabetes and Endocrinology, Cairns Base Hospital, Cairns, Queensland, Australia
Department of Endocrinology and Diabetes, St Vincent's Hospital Melbourne, Melbourne, Victoria, Australia
|Citation:||Diabetes care 2018; online first: 24 January|
|Abstract:||To 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.|
|Appears in Collections:||Journal articles|
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