Chen Xiaojing, Yu Chengyuan, Jing Haijiao, Wang Chunxu, Zhao Xinyi, Zhang Jinming, Zhang Shuoqi, Liu Huan, Xie Rujuan, Shi Jialan
Department of Nephrology, The First Hospital of Harbin, Harbin Medical University China.
Department of Hematology, The First Hospital of Harbin, Harbin Medical University China.
Am J Transl Res. 2020 Dec 15;12(12):7640-7656. eCollection 2020.
Coronavirus disease 2019 (COVID-19) infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global pandemic disease with high morbidity and mortality. Inflammatory and thrombosis are its main manifestations. As an important organ of hemofiltration metabolism, the kidney is prone to blockage and destruction when filter high inflammatory and high viscous blood of COVID-19, resulting in the loss of a large amount of protein, aggravating blood concentration, and then worsening COVID-19 hypercoagulability, which may explain the phenomenon of erythrocytes aggregation blocking the capillary lumen and the main reason why the kidney has become the second largest involvement organs. Therefore, this review discusses the effects of pathophysiological mechanisms such as inflammatory storm, endothelial injury, phosphatidylserine expression, extracellular traps release on renal capillary thrombosis caused by COVID-19 infection. Meanwhile, in view of the above mechanisms, we put forward the potential targets of antithrombotic therapy, and graded management of patients, reasonable use of drugs according to the severity of the disease and the choice of time. And we support the view of prevention of thrombus before admission, continuous anticoagulation and drug choice after discharge. It is suggested that the symptomatic and supportive treatment of renal disease in critically ill patients should be combined with the concept of antithrombotic therapy. The ultimate goal is to reduce the occurrence and development of kidney disease, provide direction for the current management of COVID-19 with kidney disease, and reduce the mortality of COVID-19.
由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染引起的2019冠状病毒病(COVID-19)已成为一种发病率和死亡率都很高的全球性大流行病。炎症和血栓形成是其主要表现。肾脏作为血液滤过代谢的重要器官,在滤过COVID-19的高炎症和高黏稠血液时容易发生堵塞和破坏,导致大量蛋白质流失,加重血液浓缩,进而使COVID-19的高凝状态恶化,这可能解释了红细胞聚集阻塞毛细血管腔的现象以及肾脏成为第二大受累器官的主要原因。因此,本综述讨论了炎症风暴、内皮损伤、磷脂酰丝氨酸表达、细胞外陷阱释放等病理生理机制对COVID-19感染所致肾毛细血管血栓形成的影响。同时,针对上述机制,我们提出了抗血栓治疗的潜在靶点,以及对患者进行分级管理,根据疾病严重程度和时机选择合理用药。并且我们支持入院前预防血栓形成、出院后持续抗凝及药物选择的观点。建议危重症患者肾脏疾病的对症支持治疗应结合抗血栓治疗理念。最终目标是减少肾脏疾病的发生和发展,为目前COVID-19合并肾脏疾病的管理提供方向,降低COVID-19的死亡率。