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                <text>Coronavirus</text>
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                <text>Dominio científico: Coronavirus</text>
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              <text>Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury.</text>
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              <text>Junzhe Chen, Wenbiao Wang, Ying Tang, Xiao-Ru Huang, Xueqing Yu, Hui-Yao Lan</text>
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              <text>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.</text>
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              <text>2021</text>
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              <text>Cytokines, inflammation, covid-19, mechanisms, AKI</text>
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              <text>10.7150/ijbs.58791</text>
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              <text>International journal of biological sciences</text>
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