THE ROLE OF TUMOUR NECROSIS FACTOR RECEPTOR 1 (TNFR1) IN THE PROGRESSION OF KIDNEY DISEASE IN INDIGENOUS AUSTRALIANS: THE EGFR FOLLOW-UP STUDY

ELM BARR1,2, F BARZI1, JT HUGHES1,3, G JERUMS4,5, WE HOY6, K O’DEA7, GRD JONES8.9, PD LAWTON1, ADH BROWN7,10, EI EKINCI1,4,5, A SINHA11, A CASS1, RJ MACISAAC5,12, LJ MAPLE-BROWN1,3

1 Menzies School of Health Research, Darwin, Northern Territory; 2Baker Heart and Diabetes Institute, Melbourne, Victoria; 3Royal Darwin Hospital, Darwin, Northern Territory; 4Austin Health, Department of Endocrinology, Melbourne, Victoria; 5University of Melbourne, Department of Medicine, Melbourne, Victoria; 6The University of Queensland, Brisbane, Queensland; 7University of South Australia, Nutrition and Population Health, Adelaide, South Australia; 8St Vincent’s Hospital, SydPath, Sydney, New South Wales; 9University of New South Wales, Department of Medicine, Sydney, New South Wales; 10South Australian Health and Medical Research Institute, Indigenous Health, Adelaide, South Australia; 11Cairns Base Hospital, Diabetes and Endocrinology, Cairns, Queensland; 12St Vincent’s Hospital Melbourne, Melbourne, Victoria.

Aim: To examine the relationship between tumour necrosis factor receptor 1 (TNFR1) and estimated glomerular filtration rate (eGFR) decline in Indigenous Australians.

Background: TNFR1 is a marker of chronic inflammation and predicts eGFR decline in people with diabetes. However, its role in Indigenous Australians with and without diabetes is not understood.

Methods: Between 2007 and 2011, 654 Indigenous men and women were recruited from urban, regional and remote Australia across diabetes and/or kidney function strata. Baseline measures included: TNFR1, serum creatinine, urine albumin-to-creatinine ratio (uACR) and HbA1c. Diabetes was classified as present (HbA1c ≥ 6.5% or physician-diagnosed diabetes) or absent (HbA1c <6.5 %). eGFR was determined using the Chronic Kidney Disease Epidemiology Collaboration (CKD-Epi) equation. Annual CKD-Epi eGFR change (ml/min/1.73m2/year) was calculated as follow-up CKD-Epi eGFR minus baseline CKD-Epi / follow-up time. Follow-up data were available for 550, and 470 had complete data on TNFR1, CKD-Epi eGFR, albuminuria and diabetes. Linear regression estimated eGFR change for quartiles (Q) of increasing TNFR1 adjusting for age, sex, CKD-Epi eGFR and uACR.

Results: Over a median of 3 years, there was no association between increasing TNFR1 and eGFR decline for those without diabetes (n=267). Among those with diabetes (n=203), compared to TNFR1 Q1 (773-1282 pg/ml), the eGFR decline (ml/min/1.73m2/year) was: -0.3 (95% CI -3.1 to 2.5; p=0.842) for Q2 (1283-1624 pg/ml), -1.1 (-3.8 to 1.6; p=0.436) for Q3 (1625-2136 pg/ml) and -5.2 (-8.1 to -2.2; p=0.001) for Q4 (2153-9264 pg/ml). Further adjustment for uACR attenuated the relationship for Q4 but it remained significant (-3.5; -6.4 to -0.5; p=0.022).

Conclusions: Higher baseline TNFR1 levels are associated with progression of kidney disease in Indigenous Australians with diabetes independent of albuminuria.

About ANZSN

The ASM is hosted by Australian and New Zealand Society of Nephrology.

The aims of the Society are to promote and support the study of the kidney and urinary tract in health and disease, and to ensure the highest professional standards for the practice of nephrology in Australia and New Zealand.

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