Departments of Biochemistry and Medicine, University College of Medical Sciences (University of Delhi) & GTB Hospital, Delhi, 110095 India.
J Diabetes Complications. 2013 Nov-Dec;27(6):548-52. doi: 10.1016/j.jdiacomp.2013.07.005. Epub 2013 Sep 6.
Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide. It results from diverse etiologies, diabetes being a frontrunner amongst them. Type 2 diabetes mellitus (DM) is being increasingly recognized as a proinflammatory state with increased oxidative stress which enormously increases the risk of micro and macro vascular diseases. This study was planned to explore the possible association between tumor necrosis factor-alpha (TNF-α), urinary monocyte chemoattractant protein-1 (uMCP-1), high-sensitivity C-reactive protein (hsCRP) and parameters of oxidative stress in patients with Type 2 diabetes mellitus (DM) and diabetic chronic kidney disease (DM-CKD). Fifty patients each were recruited in DM, DM-CKD and healthy control groups. Plasma TNF-α, hsCRP and uMCP-1 levels as inflammatory mediators were measured by ELISA, reduced glutathione (GSH), ferric reducing ability of plasma (FRAP) as parameters of antioxidant activity and malondialdehyde (MDA) as marker of oxidative stress, were measured spectrophotometrically. Plasma TNF-α, hsCRP and uMCP-1 were significantly higher in DM-CKD compared to DM and healthy controls. Lipid peroxidation, measured as MDA was significantly higher in patients with DM-CKD as compared to patients with DM and healthy controls. Further, antioxidant capacity of blood measured as FRAP and GSH was found to be significantly lower in patients with DM and DM-CKD as compared to healthy controls (p<0.001). Plasma TNF-α and uMCP-1 showed a significant positive correlation with HbA1c (r=0.441, 0.643), hsCRP (r=0.400, 0.584) and MDA (r=0.423, 0.759) and significant negative correlation with GSH (R=-0.370, -0.800) and FRAP (r=-0.344, -0.684) Increased inflammatory markers viz. TNF-α, hsCRP and uMCP-1 and markers of oxidative stress i.e. increased MDA and decreased GSH and FRAP in DM-CKD suggest an important role of inflammation and oxidative stress in the pathogenesis of renal damage in diabetic patients.
慢性肾脏病（CKD）是全球发病率和死亡率的主要原因。它由多种病因引起，其中糖尿病是主要病因之一。2 型糖尿病（DM）被认为是一种炎症状态，氧化应激增加，这极大地增加了微血管和大血管疾病的风险。本研究旨在探讨肿瘤坏死因子-α（TNF-α）、尿单核细胞趋化蛋白-1（uMCP-1）、高敏 C 反应蛋白（hsCRP）与 2 型糖尿病（DM）及糖尿病慢性肾脏病（DM-CKD）患者氧化应激参数之间的可能相关性。每组 50 例患者分别纳入 DM 组、DM-CKD 组和健康对照组。通过 ELISA 测定血浆 TNF-α、hsCRP 和 uMCP-1 等炎症介质水平，用分光光度法测定还原型谷胱甘肽（GSH）、血浆铁还原能力（FRAP）等抗氧化活性参数和丙二醛（MDA）作为氧化应激标志物。DM-CKD 组患者的血浆 TNF-α、hsCRP 和 uMCP-1 明显高于 DM 组和健康对照组。与 DM 组和健康对照组相比，DM-CKD 患者的脂质过氧化产物 MDA 明显升高。进一步发现，与健康对照组相比，DM 和 DM-CKD 患者的血液抗氧化能力 FRAP 和 GSH 明显降低（p<0.001）。血浆 TNF-α和 uMCP-1 与 HbA1c（r=0.441，0.643）、hsCRP（r=0.400，0.584）和 MDA（r=0.423，0.759）呈显著正相关，与 GSH（R=-0.370，-0.800）和 FRAP（r=-0.344，-0.684）呈显著负相关。DM-CKD 中炎症标志物 TNF-α、hsCRP 和 uMCP-1 以及氧化应激标志物 MDA 降低和 GSH、FRAP 降低，提示炎症和氧化应激在糖尿病患者肾损伤发病机制中起重要作用。
