Barr Elizabeth L M, Barzi Federica, Mills Kulkalgal Phillip, Nickels Maria, Graham Sian, Pearson Odette, Obeyesekere Varuni, Hoy Wendy E, Jones Graham R D, Lawton Paul D, Brown Alex D H, Thomas Mark, Sinha Ashim, Cass Alan, MacIsaac Richard J, Maple-Brown Louise J, Hughes Wagadagam Jaquelyne T
Menzies School of Health Research, Charles Darwin University, Casuarina, NT, Australia.
Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Can J Kidney Health Dis. 2025 Aug 17;12:20543581251363126. doi: 10.1177/20543581251363126. eCollection 2025.
Traditional markers modestly predict chronic kidney disease progression in Aboriginal and Torres Strait Islander people. Therefore, we assessed associations of cardiometabolic and inflammatory clinical biomarkers with kidney disease progression among Aboriginal and Torres Strait Islander people with and without diabetes.
To identify cardiometabolic and inflammatory clinical biomarkers that predict kidney disease progression in Aboriginal and Torres Strait Islander people.
Prospective observational cohort study.
Northern Territory, Australia.
Aboriginal and Torres Strait Islander participants of the estimated glomerular filtration rate (eGFR) study with (n = 218) and without diabetes (n = 278).
Baseline biomarkers (expressed as 1 standard deviation increase in logarithmic scale), plasma kidney injury molecule-1 (pKIM-1) (pg/ml), high-sensitivity troponin-T (hs-TnT) (ng/L), troponin-I (hs-TnI) (ng/L), and soluble tumor necrosis factor receptor-1 (sTNFR-1) (pg/ml) were assessed in 496 adults. Annual change in eGFR (ml/min/1.73 m) and a composite kidney outcome (first of ≥30% eGFR decline with follow-up eGFR <60 ml/min/1.73 m, initiation of kidney replacement therapy or kidney disease-related death) over a median of 3 years.
Linear regression estimated annual change in eGFR (ml/min/1.73 m). Cox proportional hazards regression estimated hazard ratio (HR) and 95% CI for developing a combined kidney health outcome.
In individuals with diabetes, but not those without diabetes, higher baseline hs-TnT (-2.1 [-4.1 to -0.2], = .033) and sTNFR-1 (-1.8 [-3.5 to -0.1], = .039) predicted mean (95% CI) eGFR change, after adjusting for age, gender, baseline eGFR, and urinary albumin-to-creatinine ratio. Baseline variables explained 11% of eGFR decline variance; increasing to 27% ( < .001) with biomarkers. In diabetes, hs-TnT and hs-TnI were significantly associated with increased risk of kidney health outcomes.
Limitations included potential chronic kidney disease misclassification from single creatinine and albumin measurements, limited adjustment for covariates due to a small sample size, and short follow-up restricting long-term outcome assessment.
Cardiovascular, kidney, and inflammatory biomarkers are likely associated with kidney function loss in diabetes, with particularly prominent associations for cardiac injury markers.
传统标志物对原住民和托雷斯海峡岛民慢性肾病进展的预测能力有限。因此，我们评估了合并或未合并糖尿病的原住民和托雷斯海峡岛民中心血管代谢及炎症临床生物标志物与肾病进展之间的关联。
确定能够预测原住民和托雷斯海峡岛民肾病进展的心血管代谢及炎症临床生物标志物。
前瞻性观察队列研究。
澳大利亚北领地。
估算肾小球滤过率（eGFR）研究中的原住民和托雷斯海峡岛民参与者，其中合并糖尿病者（n = 218），未合并糖尿病者（n = 278）。
对496名成年人评估基线生物标志物（以对数尺度表示为1个标准差增加）、血浆肾损伤分子-1（pKIM-1）（pg/ml）、高敏肌钙蛋白T（hs-TnT）（ng/L）、肌钙蛋白I（hs-TnI）（ng/L）和可溶性肿瘤坏死因子受体-1（sTNFR-1）（pg/ml）。随访3年期间eGFR（ml/min/1.73 m²）的年变化量以及复合肾脏结局（首次出现eGFR下降≥30%且随访时eGFR < 60 ml/min/1.73 m²、开始肾脏替代治疗或肾病相关死亡）。
线性回归估计eGFR（ml/min/1.73 m²）的年变化量。Cox比例风险回归估计发生复合肾脏健康结局的风险比（HR）及95%置信区间（CI）。
在合并糖尿病的个体中，而非未合并糖尿病的个体中，校正年龄、性别、基线eGFR和尿白蛋白与肌酐比值后，较高的基线hs-TnT（-2.1 [-4.1至-0.2]，P = 0.033）和sTNFR-1（-1.8 [-3.5至-0.1]，P = 0.039）可预测平均（95%CI）eGFR变化。基线变量解释了eGFR下降方差的11%；加入生物标志物后增至27%（P < 0.001）。在糖尿病患者中，hs-TnT和hs-TnI与肾脏健康结局风险增加显著相关。
局限性包括单次肌酐和白蛋白测量可能导致慢性肾病误诊、样本量小导致协变量调整有限以及随访时间短限制了长期结局评估。
心血管、肾脏和炎症生物标志物可能与糖尿病患者的肾功能丧失有关，心脏损伤标志物的关联尤为突出。
