期刊
DIABETES CARE
卷 41, 期 4, 页码 739-747出版社
AMER DIABETES ASSOC
DOI: 10.2337/dc17-1919
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资金
- National Health and Medical Research Council (NHMRC) [545202, 1021460]
- SVHA Inclusive Health Innovation Fund
- Kidney Health Australia
- NHMRC [631947, 1092576, 1120640, 605837, 1078477]
- Colonial FoundationRoyal Australasian College of Physicians Jacquot Research Establishment Award
- Diabetes Australia Research TrustNHMRC-funded Centre for Research Excellence in Chronic Kidney Disease [1079502]
- Rebecca L. Cooper Foundation
- SeaSwift Thursday Island
- NHMRC Training Research Fellowship [APP1016612]
- National Heart Foundation of Australia post-doctoral fellowship [1012914]
- Viertel Senior Medical Research Fellowship from the Sylvia and Charles Viertel Charitable Foundation
- NHMRC Early Career Fellowship (the Health Professional Research Fellowship) [1054312]
- Royal Australasian College of Physicians JDRF Research Establishment Fellowship
- Sir Edward Weary Dunlop Medical Research Foundation
- Australian Diabetes Society-Servier Diabetes Research Fellowship
OBJECTIVETo 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.RESEARCH DESIGN AND METHODSThis 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), HbA(1c), 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 m(2), progression to renal replacement therapy, or renal death) for increasing sTNFR1.RESULTSOver 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 m(2)/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).CONCLUSIONSsTNFR1 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.
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