C-reactive protein, oxidative stress, homocysteine, and troponin as inflammatory and metabolic predictors of atherosclerosis in ESRD.
C-reactive protein, oxidative stress, homocysteine, and troponin as inflammatory and metabolic predictors of atherosclerosis in ESRD.
复制标题
C 反应蛋白、氧化应激、同型半胱氨酸和肌钙蛋白作为 ESRD 动脉粥样硬化的炎症和代谢预测因子。
DOI：
10.1097/00041552-200011000-00006
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发表时间：
2000
影响因子：
3.2
通讯作者：
Kaysen,GA
中科院分区：
文献类型：
--
作者：
Yeun,JY;Kaysen,GA
终末期肾病患者的死亡率仍然很高，心血管疾病占这些死亡的一半。新的危险因素，如炎症，氧化应激，高同型半胱氨酸血症和高肌钙蛋白水平与一般人群的心血管风险有关。虽然有大量流行病学数据证实这些新的风险因素与终末期肾病患者的心血管风险相关，但尚未建立因果关系。炎症很容易通过高水平的C反应蛋白的存在来识别，而氧化应激的研究由于缺乏标准化测试而受到阻碍。两者的原因都是未知的。高同型半胱氨酸血症是由于甲硫氨酸再甲基化减少所致，尽管补充维生素只能部分纠正这一缺陷，这表明尿毒症对酶促过程的抑制可能很重要。纠正氧化应激和高同型半胱氨酸血症最有前途的策略分别是维生素E和亚叶酸治疗。肌钙蛋白I似乎是比肌钙蛋白T更特异的心肌损伤标志物，但肌钙蛋白T保留了其预测心血管死亡率以及全因死亡率的能力。由于这些因素可能相互影响，可能会增加氧化应激，并可能通过脂质的氧化修饰介导动脉粥样硬化，因此很难区分这些风险因素中的每一个的作用。
Mortality in patients with end-stage renal disease remains high, with cardiovascular disease accounting for half of these deaths. Novel risk factors such as inflammation, oxidative stress, hyperhomocysteinemia, and high troponin levels are associated with cardiovascular risk in the general population. While there are substantial epidemiologic data confirming that these novel risk factors are associated with cardiovascular risk in end-stage renal disease patients, a causal relationship has not been established. Inflammation is readily identified by the presence of high levels of C-reactive protein, while studies of oxidative stress are hampered by the lack of a standardized test. The cause of both is unknown. Hyperhomocysteinemia results from decreased remethylation to methionine, although vitamin supplementation only partially corrects the defect, suggesting that uremic inhibition of the enzymatic process may be important. The most promising strategies for correcting oxidative stress and hyperhomocysteinemia are vitamin E and folinic acid therapy, respectively. Troponin I appears to be a more specific marker of myocardial injury than Troponin T, but troponin T retains its ability to predict cardiovascular mortality as well as all-cause mortality. Sorting out the role of each of these risk factors may be difficult since the factors may influence each other, may increase oxidative stress, and may mediate atherosclerosis through oxidative modification of lipids.