Background and purpose Non-traditional risk factors such as chronic inflammation, oxidative stress and thrombogenic factors are believed to contribute to the excess stroke risk in chronic kidney disease (CKD) by triggering vascular injury and endothelial dysfunction. We aimed to determine how well a panel of biomarkers representative of these factors would correlate with estimated glomerular filtration rate (eGFR) in patients with recent transient ischaemic attack (TIA) or stroke. We also investigated whether eGFR would confound previously reported associations between biomarkers and mortality. Methods We studied a panel of 16 blood biomarkers related to inflammation, thrombosis, atherogenesis and cardiac or neuronal cell damage in TIA or ischaemic stroke in a population-based study (Oxford Vascular Study). Biomarker levels were log-transformed and correlated with eGFR, adjusted for age. Cox proportional hazard models were used for survival analysis. Results Among 1297 patients with TIA or stroke, 52.7% (n=684) of patients had CKD (eGFR <60 mL/min/1.73 m2). There was a moderate correlation between log-eGFR and the log-transformed soluble tumour necrosis factor receptor-1 (R2=0.21), attenuating with adjustment for age (R2=0.12). There were moderate-to-strong correlations with markers of cardiac injury, N-terminal pro-brain natriuretic peptide and heart-type fatty acid binding protein (hFABP, R2=0.14 and 0.34, respectively). The strongest correlation after adjustment for age was between hFABP and eGFR (R2=0.20). Adjusting for eGFR did not impact any biomarker associations with mortality. Conclusions Correlations between biomarkers related to inflammation and thrombosis with renal dysfunction in the setting of cerebrovascular events were generally modest after adjustment for age, suggesting that putative risk factors such as chronic inflammation or coagulopathy are unlikely to be important stroke mechanisms in patients with CKD.

中文翻译：

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TIA 和中风患者血液生物标志物与肾小球滤过率的关联：基于人群的研究

背景和目的 非传统危险因素，如慢性炎症、氧化应激和血栓形成因素被认为通过引发血管损伤和内皮功能障碍而导致慢性肾病 (CKD) 中风风险过高。我们旨在确定代表这些因素的一组生物标志物与近期短暂性脑缺血发作 (TIA) 或中风患者的估计肾小球滤过率 (eGFR) 的相关性如何。我们还调查了 eGFR 是否会混淆先前报道的生物标志物与死亡率之间的关联。方法 我们在一项基于人群的研究（牛津血管研究）中研究了一组 16 种与 TIA 或缺血性中风中的炎症、血栓形成、动脉粥样硬化形成和心脏或神经元细胞损伤相关的血液生物标志物。生物标志物水平经过对数转换并与 eGFR 相关，并根据年龄进行了调整。Cox比例风险模型用于生存分析。结果 在 1297 例 TIA 或卒中患者中，52.7%（n=684）的患者患有 CKD（eGFR <60 mL/min/1.73 m2）。log-eGFR 与对数转化的可溶性肿瘤坏死因子受体-1 之间存在中度相关性（R2=0.21），随着年龄的调整而减弱（R2=0.12）。与心脏损伤标志物、N末端脑利钠肽前体和心脏型脂肪酸结合蛋白（hFABP，R2分别为0.14和0.34）存在中度至强相关性。调整年龄后最强的相关性在 hFABP 和 eGFR 之间（R2=0.20）。调整 eGFR 并未影响任何与死亡率相关的生物标志物。