Malyszko J, Malyszko J S, Pawlak D, Pawlak K, Buczko W, Mysliwiec M
Department of Nephrology, Bialystok Medical School, Poland.
Thromb Res. 1996 Sep 1;83(5):351-61. doi: 10.1016/0049-3848(96)00145-4.
A pathogenetic role for fibrin deposition and platelet activation in the kidney is thought to play a role in the pathogenesis of acute renal failure (ARF). Thus, some fibrinolytic parameters and platelet function have been studied in 17 patients with ARF and compared to healthy volunteers and subjects with chronic renal failure (CRF). Since serotonin may participate in pathological processes resulting from platelet/vessel wall interactions, its level in the whole blood and plasma was also assayed. In ARF and CRF platelet aggregatory responses in both whole blood and in platelet rich plasma upon stimulation with various agonists (collagen, arachidonic acid, ADP, ristocetin) were lower than those obtained in healthy volunteers. Increased levels of lipoprotein (a), von Willebrand factor (vWF) and fibronectin were found in ARF relative to controls. Protein C activity was significantly lower in patients with ARF. Euglobulin clot lysis time was prolonged in ARF and CRF, reflecting a decreased overall fibrinolytic activity. Activity of tissue plasminogen activator (tPA) inhibitor (PAI) and PAI:Ag were higher in ARF, whereas tPA:Ag, urokinase, tPA/PAI complexes, thrombin-antithrombin complexes (TAT), plasmin-antiplasmin (PAP) complexes, fibrinogen, and F1+2 did not differ between ARF and controls. In CRF elevated levels of TAT, PAP, fibrinogen and prothrombin fragments F1+2 were found, whereas concentration of fibronectin was lowered when compared to controls. In both groups of renal failure patients increased levels of fibrin monomers and d-dimer were found relative to healthy volunteers. Whole blood serotonin was significantly lower, whereas plasma serotonin was significantly higher in patients with ARF and CRF relative to controls. Serotonin uptake and its release from platelets were markedly diminished in patients with ARF and CRF. Chronic renal failure exhibit a slightly different pattern of coagulopathies that acute renal failure.
纤维蛋白沉积和血小板激活在肾脏中的致病作用被认为在急性肾衰竭（ARF）的发病机制中发挥作用。因此，对17例ARF患者的一些纤溶参数和血小板功能进行了研究，并与健康志愿者和慢性肾衰竭（CRF）患者进行了比较。由于血清素可能参与血小板/血管壁相互作用导致的病理过程，还检测了全血和血浆中血清素的水平。在ARF和CRF中，用各种激动剂（胶原、花生四烯酸、ADP、瑞斯托霉素）刺激后，全血和富含血小板血浆中的血小板聚集反应均低于健康志愿者。与对照组相比，ARF患者脂蛋白（a）、血管性血友病因子（vWF）和纤连蛋白水平升高。ARF患者蛋白C活性显著降低。ARF和CRF患者优球蛋白凝块溶解时间延长，反映总体纤溶活性降低。ARF患者组织型纤溶酶原激活物（tPA）抑制剂（PAI）活性和PAI:Ag较高，而tPA:Ag、尿激酶、tPA/PAI复合物、凝血酶-抗凝血酶复合物（TAT）、纤溶酶-抗纤溶酶（PAP）复合物、纤维蛋白原和F1+2在ARF和对照组之间无差异。在CRF中，发现TAT、PAP、纤维蛋白原和凝血酶原片段F1+2水平升高，而与对照组相比，纤连蛋白浓度降低。与健康志愿者相比，两组肾衰竭患者的纤维蛋白单体和D-二聚体水平均升高。ARF和CRF患者的全血血清素显著降低，而血浆血清素显著高于对照组。ARF和CRF患者血小板对血清素的摄取及其释放明显减少。慢性肾衰竭表现出与急性肾衰竭略有不同的凝血病模式。
