Int J Biol Sci 2021; 17(6):1497-1506. doi:10.7150/ijbs.58791

Review

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

Junzhe Chen1,2, Wenbiao Wang1,3, Ying Tang2, Xiao-ru Huang1,4, Xueqing Yu4, Hui-Yao Lan1,5✉

1. Departments of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, and Lui Che Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Hong Kong, China.
2. Department of Nephrology, The Third Affiliated hospital, Southern Medical university, Guangzhou, China.
3. Guangdong Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Guangzhou, China.
4. Guangdong-Hong Kong Joint Laboratory for Immunity and Genetics of Chronic Kidney Disease, Guangdong Academy of Medical Science, Guangdong Provincial People's Hospital, Guangzhou, China.
5. Guangdong-Hong Kong Joint Laboratory for Immunity and Genetics of Chronic Kidney Disease, The Chinese University of Hong Kong, Hong Kong, China.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Citation:
Chen J, Wang W, Tang Y, Huang Xr, Yu X, Lan HY. Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury. Int J Biol Sci 2021; 17(6):1497-1506. doi:10.7150/ijbs.58791. Available from https://www.ijbs.com/v17p1497.htm

File import instruction

Abstract

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-β 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-β OT-101, and the use of CRRT in critically ill patients may represent as novel and specific therapies for AKI in COVID-19 patients.

Keywords: COVID-19, AKI, cytokines, inflammation, mechanisms