Yao Qiang, Pecoits-Filho Roberto, Lindholm Bengt, Stenvinkel Peter
Renal Division, Renji Hospital, Shanghai Second Medical University, Shanghai, People's Republic of China.
Scand J Urol Nephrol. 2004;38(5):405-16. doi: 10.1080/00365590410031715.
Cardiovascular disease (CVD) remains the main cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Although traditional risk factors, such as diabetes mellitus, hypertension, dyslipidemia and advanced age, are prevalent in ESRD patients they may not be sufficient by themselves to account for the high prevalence of CVD in patients with this condition. Thus, the search for other, non-traditional, risk factors that may be involved in the pathogenesis of uremic CVD has been an area of intense study. Data suggest that the accelerated atherosclerotic process of ESRD may involve several interrelated processes, such as oxidative stress, endothelial dysfunction and vascular calcification, in a milieu of constant low-grade inflammation. The cause(s) of inflammation in ESRD are multifactorial and, while it may reflect underlying CVD, an acute-phase reaction may also be a direct cause of vascular injury via several pathogenetic mechanisms. Available data suggest that pro-inflammatory cytokines play a central role in the genesis of both malnutrition and CVD in ESRD. Thus, it could be speculated that suppression of the vicious cycle of malnutrition, inflammation and atherosclerosis (MIA syndrome) would improve survival in dialysis patients. Recent evidence has demonstrated strong associations between inflammation and both increased oxidative stress and endothelial dysfunction in ESRD patients. As there is not yet any recognized, or even proposed, treatment for ESRD patients with chronic inflammation it would be of obvious interest to study the long-term effect of various anti-inflammatory treatment strategies on the nutritional and cardiovascular status as well as outcome of these patients.
心血管疾病（CVD）仍然是终末期肾病（ESRD）患者发病和死亡的主要原因。尽管传统危险因素，如糖尿病、高血压、血脂异常和高龄，在ESRD患者中普遍存在，但它们本身可能不足以解释这种情况下CVD的高患病率。因此，寻找可能参与尿毒症性CVD发病机制的其他非传统危险因素一直是一个深入研究的领域。数据表明，ESRD加速的动脉粥样硬化过程可能涉及几个相互关联的过程，如氧化应激、内皮功能障碍和血管钙化，处于持续的低度炎症环境中。ESRD炎症的原因是多因素的，虽然它可能反映潜在的CVD，但急性期反应也可能通过几种发病机制直接导致血管损伤。现有数据表明，促炎细胞因子在ESRD患者营养不良和CVD的发生中起核心作用。因此，可以推测，抑制营养不良、炎症和动脉粥样硬化的恶性循环（MIA综合征）将提高透析患者的生存率。最近的证据表明，炎症与ESRD患者氧化应激增加和内皮功能障碍之间存在密切关联。由于目前尚无针对慢性炎症的ESRD患者的公认治疗方法，甚至也没有提出相关治疗方法，因此研究各种抗炎治疗策略对这些患者的营养和心血管状况以及预后的长期影响将具有明显的意义。
