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糖尿病(DM)已成为世界性的常见病,其发病率高,并且随着生活水平的改善,其发病率必然还会进一步加剧。血管病变是DM的重要并发症之一,糖尿病肾病(DN)是糖尿病常见且严重的微血管并发症,与血栓形成密切相关。糖尿病肾病的进展伴随着体内凝血活性和抗凝活性的失调,同时激活自身免疫系统,发生炎症反应。炎症应答过程中释放的炎症因子损伤肾小球内皮细胞,导致抗凝活性减弱。DN患者体内血细胞激活,微粒形成增多会加强凝血活性。此外,纤溶酶抑制剂(PAI-1)与纤溶酶激活剂(t PA)的失衡会引起纤溶系统紊乱。这三个方面引起DN患者体内的高凝状态加重,并因此加速肾功能恶化,导致肾小球率过滤降低,系膜基质增多,最终引起肾小球硬化及终末期肾脏疾病。本文就糖尿病肾病致凝血异常的发生机制做一综述。
Diabetes mellitus (DM) has become a worldwide endemic disease with a high incidence, and its incidence will inevitably further increase as the standard of living is improved. Vascular disease is one of the important complication of DM. Diabetic nephropathy (DN) is a common and serious microvascular complication of diabetes mellitus, which is closely related to thrombosis. The progression of diabetic nephropathy is accompanied by an imbalance of coagulation activity and anticoagulant activity in vivo, while activating the autoimmune system and causing an inflammatory reaction. Inflammatory factors released during inflammatory response damage glomerular endothelial cells, resulting in diminished anticoagulant activity. DN patients with blood cell activation, increased particle formation will enhance coagulation activity. In addition, an imbalance between plasmin inhibitor (PAI-1) and plasmin activator (t PA) can cause fibrinolytic disorders. These three aspects cause aggravation of the hypercoagulable state in patients with DN and thus exacerbate the worsening of renal function, leading to a decrease in the filtration of the glomeruli and an increase in the mesangial matrix, which eventually leads to glomerulosclerosis and end-stage renal disease. This article reviews the mechanism of coagulopathy caused by diabetic nephropathy.