Bobrova L A, Kozlovskaya N L
Sechenov First Moscow State Medical University (Sechenov University).
People's Friendship University of Russia.
Ter Arkh. 2020 Jul 9;92(6):105-116. doi: 10.26442/00403660.2020.06.000667.
This review devoted to the nephrotic syndrome (NS) subsequent thrombotic outcomes. The pathogenesis of hypercoagulation disorders that cause venous and arterial vascular system thrombosis are studied. Discussed procoagulant and anticoagulant mechanisms imbalance due to the anticoagulants natural urinal loss, affected by disfunction of the glomerular filter selective permeability, leading to high molecular weight liver-derived proteins (at least of the albumin size) leakage, fibrinolysis depression, excessive liver synthesis of plasma clotting cascade factors and platelet activation. Presented new data on the thrombogenesis at NS concerning the role of endothelial microparticles with high prothrombogenic activity that go from damaged glomerulus endothelial capillary cells into the systemic circulation, which can turn the local renal hypercoagulation (concomitant to the kidney immune inflammation process) into the generalized, working towards the thrombosis development. The most frequent adverse variants of arterial and venous thromboses are studied, specified their basic and general risk factors, as well as individual, varying in different patients. Indications and prophylactic anticoagulant therapy regimen and thrombosis treatment duration in patients with NS are discussed. It also stressed that the decision on time and method of anticoagulant therapy for a NS patients is still a challenge for healthcare providers.
本综述致力于肾病综合征(NS)后续的血栓形成结局。研究了导致静脉和动脉血管系统血栓形成的高凝紊乱的发病机制。讨论了由于抗凝剂经尿液自然流失、受肾小球滤过器选择性通透性功能障碍影响,导致高分子量肝脏衍生蛋白(至少白蛋白大小)泄漏、纤维蛋白溶解抑制、血浆凝血级联因子肝脏过度合成以及血小板活化而引起的促凝和抗凝机制失衡。介绍了关于NS血栓形成的新数据,涉及具有高促血栓形成活性的内皮微粒从受损的肾小球内皮毛细血管细胞进入体循环的作用,这可将局部肾脏高凝状态(伴随肾脏免疫炎症过程)转变为全身性的,促使血栓形成。研究了动脉和静脉血栓形成最常见的不良变体,明确了其基本和一般危险因素,以及不同患者个体存在差异的危险因素。讨论了NS患者的抗凝治疗适应证、预防方案以及血栓治疗持续时间。还强调了对于NS患者,决定抗凝治疗的时间和方法对医疗服务提供者而言仍是一项挑战。