Himmelfarb Jonathan
Division of Nephrology and Transplantation, Maine Medical Center, 22 Bramhall Street, Portland, ME 04102, USA.
Cardiol Clin. 2005 Aug;23(3):319-30. doi: 10.1016/j.ccl.2005.03.005.
Patients with uremia (whether requiring renal replacement therapy or not) have a greatly increased cardiovascular risk that cannot be explained entirely by traditional cardiovascular risk factors. An increase in oxidative stress has been proposed as a nontraditional cardiovascular risk factor in this patient population. Using a wide variety of different biomarkers of increased oxidative stress status, numerous laboratories around the world have now unequivocally demonstrated that uremia is a state of increased oxidative stress. Recent data also suggest linkages between oxidative stress inflammation, endothelial dysfunction, and malnutrition in the uremic population. These factors are probably synergistic in their effects on atherogenecity and risk of a cardiovascular event. The pathophysiology of increased oxidative stress in uremia is multifactorial, but the retention of oxidized solute by the loss of kidney function is probably a major contributor. Uremic oxidative stress can be characterized biologically by an increase in lipid per oxidation products and reactive aldehyde groups as well as by increased retention of oxidized thiols. Two recently published studies have suggested that antioxidative therapy may be particularly promising in reducing cardiovascular events in this patient population.Further definitive studies of antioxidant use are greatly needed.
尿毒症患者（无论是否需要肾脏替代治疗）心血管风险大幅增加，而传统心血管危险因素无法完全解释这一现象。氧化应激增加被认为是该患者群体的一种非传统心血管危险因素。世界各地众多实验室通过使用多种不同的氧化应激状态增加的生物标志物，现已明确证明尿毒症是一种氧化应激增加的状态。近期数据还表明，尿毒症患者体内氧化应激、炎症、内皮功能障碍和营养不良之间存在联系。这些因素对动脉粥样硬化形成和心血管事件风险的影响可能具有协同作用。尿毒症中氧化应激增加的病理生理学是多因素的，但肾功能丧失导致氧化溶质潴留可能是主要原因。尿毒症氧化应激在生物学上的特征是脂质过氧化产物和活性醛基增加，以及氧化硫醇潴留增加。最近发表的两项研究表明，抗氧化治疗在降低该患者群体的心血管事件方面可能特别有前景。非常需要对抗氧化剂使用进行进一步的确定性研究。
