Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury

作者：Chen, Junzhe; Wang, Wenbiao; Tang, Ying; Huang, Xiao-Ru; Yu, Xueqing; Lan, Hui-Yao^*

来源：International Journal of Biological Sciences, 2021, 17(6): 1497-1506.

DOI：10.7150/ijbs.58791

• COVID-19
• AKI
• cytokines
• inflammation
• mechanisms

Increasing clinical evidence shows that acute kidney injury (AKI) is a common and severe complication in critically ill COVID-19 patients. The older age, the severity of COVID-19 infection, the ethnicity, and the history of smoking, diabetes, hypertension, and cardiovascular disease are the risk factor for AKI in COVID-19 patients. Of them, inflammation may be a key player in the pathogenesis of AKI in patients with COVID-19. It is highly possible that SARS-COV-2 infection may trigger the activation of multiple inflammatory pathways including angiotensin II, cytokine storm such as interleukin-6 (IL-6), C-reactive protein (CRP), TGF-8 signaling, complement activation, and lung-kidney crosstalk to cause AKI. Thus, treatments by targeting these inflammatory molecules and pathways with a monoclonal antibody against IL-6 (Tocilizumab), C3 inhibitor AMY-101, anti-C5 antibody, anti-TGF-8 OT-101, and the use of CRRT in critically ill patients may represent as novel and specific therapies for AKI in COVID-19 patients.

• 单位
  河北医科大学; 广东省人民医院; 南方医科大学