Wang Mo, Xiong Huaying, Chen Han, Li Qiu, Ruan Xiong Zhong
Department of Nephrology, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Key Laboratory of Pediatrics, Chongqing, China.
Kidney Dis (Basel). 2021 Mar;7(2):100-110. doi: 10.1159/000512683. Epub 2020 Nov 16.
SARS-CoV-2 infection can cause renal involvement, and severe renal dysfunction is more common among patients with chronic comorbid conditions, especially patients with chronic kidney disease. Angiotensin-converting enzyme 2 (ACE2) has been proven to be the major receptor of SARS-CoV-2 in kidneys, suggesting that ACE2-related changes may be involved in renal injury during the infection. In this review, we systematically reviewed the literature to summarize findings on the mechanism of renal injury caused by SARS-COV-2 infection, in order to provide a theoretical basis for renal protection therapy.
For patients with SARS-CoV-2 infection, renal injury mainly manifests as increased serum creatinine, variable degrees of proteinuria and hematuria, and radiographic abnormalities of the kidneys. In this review, we summarize the pathogenesis of renal injury deriving from SARS-CoV-2 infection by focusing on its etiology, pathology, and clinical manifestations. The virus causes kidney injury by either direct infection or systemic effects, including host immune clearance and immune tolerance disorders, endothelium-mediated vasculitis, thrombus formation, glucose and lipid metabolism disorder, and hypoxia.
Renal injury by SARS-CoV-2 is the result of multiple factors. Via highly expressed ACE2 in renal tissue, SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury. Systemic effects such as host immune clearance and immune tolerance disorders, endothelial cell injury, thrombus formation, glucose and lipid metabolism disorder, and hypoxia aggravate this renal injury.
新型冠状病毒2型（SARS-CoV-2）感染可导致肾脏受累，严重肾功能不全在患有慢性合并症的患者中更为常见，尤其是慢性肾脏病患者。血管紧张素转换酶2（ACE2）已被证实是SARS-CoV-2在肾脏中的主要受体，这表明与ACE2相关的变化可能参与感染期间的肾损伤。在本综述中，我们系统回顾了文献，总结了SARS-CoV-2感染导致肾损伤机制的研究结果，以便为肾脏保护治疗提供理论依据。
对于SARS-CoV-2感染患者，肾损伤主要表现为血清肌酐升高、不同程度的蛋白尿和血尿以及肾脏影像学异常。在本综述中，我们通过关注其病因、病理和临床表现，总结了SARS-CoV-2感染导致肾损伤的发病机制。该病毒通过直接感染或全身效应导致肾损伤，包括宿主免疫清除和免疫耐受紊乱、内皮介导的血管炎、血栓形成、糖脂代谢紊乱和缺氧。
SARS-CoV-2导致的肾损伤是多种因素的结果。SARS-CoV-2感染通过肾组织中高表达的ACE2从根本上启动了肾损伤机制。宿主免疫清除和免疫耐受紊乱、内皮细胞损伤、血栓形成、糖脂代谢紊乱和缺氧等全身效应加剧了这种肾损伤。
