E BARR1,2, J HUGHES1,3, F BARZI1,4, V OBEYESEKERE5, W HOY 6, K O’DEA1, G JONES7,8, P LAWTON1,9, A BROWN10,11, M THOMAS12, A SINHA13, A CASS1, M NICKELS1, R MACISAAC5,14, L MAPLE-BROWN1,3
1Menzies School Of Health Research, Darwin, Australia, 2Baker Institute of Heart and Diabetes, Melbourne, Australia, 3Royal Darwin Hospital, Darwin, Australia, 4UQ Poche Centre, The University of Queensland, Brisbane, Australia, 5St Vincent’s Hospital Melbourne, Melbourne, Australia, 6The University of Queensland, Brisbane, Australia, 7St Vincent’s Hospital, SydPath, Sydney, Australia, 8University of New South Wales, Department of Medicine, Sydney, Australia, 9Monash University, Melbourne, Australia, 10South Australian Health and Medical Research Institute, Aboriginal Health Equity, Adelaide, Australia, 11The University of Adelaide, Aboriginal Research Unit, Adelaide Medical School, Adelaide, Australia, 12Royal Perth Hospital, Perth, Australia, 13Cairns Base Hospital, Diabetes and Endocrinology, Cairns, Australia, 14University of Melbourne, Department of Medicine, Melbourne, Australia
Aim: To assess associations of plasma kidney injury molecule-1 (pKIM-1), high-sensitivity troponin-T (hs-TnT), troponin-I (hs-TnI) and soluble tumor necrosis factor receptor-1 (sTNFR-1) with estimated glomerular filtration rate (eGFR) decline among Aboriginal and Torres Strait Islander adults with and without diabetes.
Background: Chronic kidney disease (CKD) and diabetes are significant health concerns for many Aboriginal and Torres Strait Islander people. Traditional markers modestly predict CKD progression, therefore assessment of other factors is warranted.
Methods: The eGFR study is a prospective cohort across diabetes and/or kidney function strata. Baseline pKIM-1, hs-TnT, hs-TnI, sTNFR-1 and urine albumin-to-creatinine ratio (uACR), and baseline and follow-up serum creatinine were measured. Linear regression estimated change in eGFR (ml/min/1.73m²/year) for pKIM-1 (pg/ml) and sTNFR-1 (pg/ml) as continuous variables, and hs-TnT (ng/L) and hs-TnI (ng/L) as categorical variables.
Results: Over 3 years, among those with diabetes (n=155), greater eGFR change was observed for greater pKIM-1 (-1.5 [95% CI: -3.2 to 0.1], p=0.07), greater sTNFR-1 (-3.6 [-6.7 to -0.4], p=0.03), for hs-TnT >5.4ng/L (-3.6 [-6.9 to -0.2], p=0.04) and hs-TnT >10.0ng/L (-6.1 [-9.8 to -2.4], p=0.001) compared to hs-TnT ≤3.0ng/L, after adjusting for baseline eGFR, uACR, age and sex. Associations remained after further adjustment for hypertension, HbA1c, adiposity or smoking. Baseline age, sex, eGFR and uACR explained 14% of the variance in eGFR decline, and adding pKIM-1, hs-TnT and sTNFR-1 increased this to 24% (p=0.02). No association between more cardio-specific hs-TnI and eGFR decline was observed. Associations with eGFR decline were not observed in those without diabetes (n=232).
Conclusions: In Aboriginal and Torres Strait Islander people with diabetes, novel cardio-metabolic and inflammatory markers are associated with kidney disease progression independent of common clinical risk markers.
Elizabeth Barr (BPod, GradDipPod, MPH, PhD) is a public health epidemiologist, and currently holds a Senior Research Fellow (Level C) appointment at Menzies School of Health Research. Elizabeth has provided research leadership on cardiovascular disease (CVD), diabetes and kidney disease epidemiology, and is interested in cardio-metabolic risk factors in kidney disease progression among Aboriginal and Torres Strait Islander people.