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10.7150/ijbs.58791 http://scihub22266oqcxt.onion/10.7150/ijbs.58791 33907513!8071761!33907513     free     free     free       Int+J+Biol+Sci 2021 ; 17 (6): 1497-1506 Nephropedia Template TP {{tp|p=33907513|t=2021. Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury |pdf=|usr=}}{{33907513}} gab.com Text Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury JO: Int J Biol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33907513 #FOAvip 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-beta 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-beta OT-101, and the use of CRRT in critically ill patients may represent as novel and specific therapies for AKI in COVID-19 patients. Twit Text FOAVip Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury ????Int J Biol Sci http://www.kidney.de/pget.php?&tw=1&pmid=33907513 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33907513 #FOAvip English Wikipedia <ref>{{Cite pmid|33907513}}</ref> Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury #MMPMID33907513 Chen J; Wang W; Tang Y; Huang XR; Yu X; Lan HY Int J Biol Sci 2021[]; 17 (6): 1497-1506 PMID33907513show ga 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-beta 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-beta OT-101, and the use of CRRT in critically ill patients may represent as novel and specific therapies for AKI in COVID-19 patients. |*Stress, Physiological[MESH] |Acute Kidney Injury/epidemiology/*etiology/therapy[MESH] |COVID-19/*complications/virology[MESH] |Complement Activation[MESH] |Cytokine Release Syndrome[MESH] |Diabetes Complications/metabolism[MESH] |Humans[MESH] |Inflammation/*etiology[MESH] |Renal Replacement Therapy[MESH]Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury (epmc).pdf DeepDyve Pubget Overpricing