论文部分内容阅读
一、肾小球疾病与凝血系统、血小板系统的关系当肾炎时,免疫复合物(IC)沉积或形成于肾小球袢后,可分别活化因子Ⅻ和内源性凝血系统。此外,来自血管壁损伤部位的组织凝血活酶以及活化的巨噬细胞释出凝血活性因子(PCA)可激活外源性凝血系统。当肾小球基底膜(GBM)发生严重病变时则断裂,纤维蛋白自肾小球袢渗入肾球囊腔内,并刺激巨噬细胞,有利于 IL—1、TNF 等介质释放。肾疾病时,血液凝血系统异常包括①纤维蛋白、Ⅷ因子沉积于肾小球血管壁;②肾皮质内可见纤溶酶原、纤溶酶原激活物在肾病变时发生变化;③血清、尿纤维蛋白和纤维蛋白降解产物(FDP)增加;④凝血因子(Ⅷ、Ⅸ、Ⅺ、Ⅻ因子)在临床或实验性肾病变时可发生变化;⑤实验动物亦证实肾炎时与血液凝血系统有关。IC 能活化血小板,使血小板凝聚,引起血小板释放介质,形成血栓。血小板及其相关物沉积于肾小球内会形成小血栓。体内外实验及肾炎患者血小板活
First, the relationship between glomerular diseases and coagulation system, platelet system When nephritis, immune complexes (IC) deposition or formed in the glomerular loop, respectively, factor Ⅻ activation and endogenous coagulation system. In addition, tissue thromboplastin from damaged vascular wall and activated macrophages release coagulation-activating factor (PCA) to activate the extrinsic coagulation system. When the glomerulus basement membrane (GBM) serious lesions are broken, fibrin from the glomerular infiltration into the renal balloon cavity, and stimulate macrophages, is conducive to IL-1, TNF and other media release. Kidney disease, blood coagulation system abnormalities include ① fibrin, Ⅷ factor deposition in the glomerular wall; ② renal cortex plasminogen can be seen, plasminogen activator changes in renal disease; ③ serum, urine Fibrin and fibrin degradation products (FDP) increased; ④ clotting factors (Ⅷ, Ⅸ, Ⅺ, Ⅻ factor) may change in clinical or experimental nephropathy; ⑤ experimental animals also confirmed nephritis and the blood coagulation system. IC can activate platelets, platelets aggregate, causing platelet release media, the formation of thrombus. Platelets and their related substances deposited in the glomerular formation of small thrombus. In vitro and in vivo experiments and glomerular platelet activity in patients with nephritis