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.
【저자키워드】 COVID-19, Inflammation, Cytokines, AKI, mechanisms, 【초록키워드】 Treatment, Cytokine storm, therapy, Pathogenesis, Tocilizumab, antibody, IL-6, SARS-COV-2 infection, monoclonal antibody, Infection, interleukin-6, C-reactive protein, cardiovascular disease, CRP, complement, cytokine, Acute kidney injury, diabetes, smoking, risk factor, hypertension, Complement activation, Ethnicity, interleukin, Critically ill, COVID-19 infection, severity of COVID-19, Older age, pathway, inhibitor, critically ill patients, COVID-19 patients, Angiotensin II, TGF-β, Signaling, Inflammatory, Pathways, Trigger, critically ill COVID-19 patients, history of smoking, (Tocilizumab), Critically ill patient, Activation, AMY-101, CRRT, clinical evidence, Increasing, inflammatory pathway, patients with COVID-19, 【제목키워드】 Stress,