Vaziri N D, Gonzales E C, Wang J, Said S
Department of Medicine, University of California, Irvine, Orange.
Am J Kidney Dis. 1994 Jun;23(6):828-35. doi: 10.1016/s0272-6386(12)80136-3.
Patients with end-stage renal disease (ESRD) are at risk of ischemic cardiovascular complications and vascular thrombosis. These observations prompted the present survey of the blood coagulation, fibrinolytic, and inhibitory proteins in a group of 31 ESRD patients and 32 normal controls. Immunologic and functional assays were used to quantitate plasma antigen concentrations and/or functional activities of factors XII, XI, IX, VIII, VII, X, II, and XIII, von Willebrand factor, fibrinogen, fibronectin, high molecular weight kininogen, D-dimer, antithrombin III, protein C, protein S, plasminogen, tissue-type plasminogen activator, plasminogen activator inhibitor, alpha 2-antiplasmin, alpha 1-antitrypsin, and alpha 2-macroglobulin as well as antiplasmin activity. The coagulant activities of factors XII, IX, X, and II were significantly reduced in ESRD patients despite their normal or increased plasma antigen concentrations. In addition, the ESRD patients showed hyperfibrinogenemia and significant elevations of plasma concentrations of D-dimer, von Willebrand factor, factor VII, and factor XIII antigens. They also exhibited significant reductions of antithrombin III, free protein S, plasminogen, and tissue-type plasminogen activator concentrations. Despite ultrafiltration, plasma factor IX activity and von Willebrand factor and fibrinogen concentrations decreased after hemodialysis with little or slight changes in other measured parameters. The ESRD patients studied here exhibited numerous abnormalities of coagulation, fibrinolytic, and inhibitory proteins at multiple levels. These abnormalities may be involved in the pathogenesis of cardiovascular complications and vascular thrombosis in this population. The precise mechanism(s) and clinical significance of the observed abnormalities are unknown and await further investigation.
终末期肾病（ESRD）患者有发生缺血性心血管并发症和血管血栓形成的风险。这些观察结果促使对31例ESRD患者和32例正常对照者进行了本次血液凝固、纤维蛋白溶解和抑制蛋白的调查。采用免疫和功能测定法对因子Ⅻ、Ⅺ、Ⅸ、Ⅷ、Ⅶ、Ⅹ、Ⅱ和ⅩⅢ、血管性血友病因子、纤维蛋白原、纤连蛋白、高分子量激肽原、D - 二聚体、抗凝血酶Ⅲ、蛋白C、蛋白S、纤溶酶原、组织型纤溶酶原激活剂、纤溶酶原激活剂抑制剂、α2 - 抗纤溶酶、α1 - 抗胰蛋白酶和α2 - 巨球蛋白的血浆抗原浓度和/或功能活性进行定量。尽管ESRD患者的血浆抗原浓度正常或升高，但其因子Ⅻ、Ⅸ、Ⅹ和Ⅱ的凝血活性显著降低。此外，ESRD患者表现为高纤维蛋白原血症，血浆D - 二聚体、血管性血友病因子、因子Ⅶ和因子ⅩⅢ抗原浓度显著升高。他们还表现出抗凝血酶Ⅲ、游离蛋白S、纤溶酶原和组织型纤溶酶原激活剂浓度的显著降低。尽管进行了超滤，但血液透析后血浆因子Ⅸ活性以及血管性血友病因子和纤维蛋白原浓度降低，而其他测量参数变化很小或略有变化。此处研究的ESRD患者在多个水平上表现出凝血、纤维蛋白溶解和抑制蛋白的众多异常。这些异常可能参与了该人群心血管并发症和血管血栓形成的发病机制。所观察到的异常的确切机制和临床意义尚不清楚，有待进一步研究。
