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10.1007/s11255-020-02579-8

http://scihub22266oqcxt.onion/10.1007/s11255-020-02579-8
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32720031!7384276!32720031
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suck abstract from ncbi

pmid32720031      Int+Urol+Nephrol 2021 ; 53 (1): 97-104
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  • The kidney, COVID-19, and the chemokine network: an intriguing trio #MMPMID32720031
  • Taverna G; Di Francesco S; Borroni EM; Yiu D; Toniato E; Milanesi S; Chiriva-Internati M; Bresalier RS; Zanoni M; Vota P; Maffei D; Justich M; Grizzi F
  • Int Urol Nephrol 2021[Jan]; 53 (1): 97-104 PMID32720031show ga
  • On December 30th 2019, some patients with pneumonia of unknown etiology were reported in the Program for Monitoring Emerging Diseases (ProMED), a program run by the International Society for Infectious Diseases (ISID), hypothesized to be related to subjects who had had contact with the seafood market in Wuhan, China. Chinese authorities instituted an emergency agency aimed at identifying the source of infection and potential biological pathogens. It was subsequently named by the World Committee on Virus Classification as 2019-nCoV (2019-novel coronavirus) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A number of studies have demonstrated that 2019-nCoV and the SARS-CoV shared the same cell entry receptor named angiotensin-converting enzyme 2 (ACE2). This is expressed in human tissues, not only in the respiratory epithelia, but also in the small intestines, heart, liver, and kidneys. Here, we examine the most recent findings on the effects of SARS-CoV-2 infection on kidney diseases, mainly acute kidney injury, and the potential role of the chemokine network.
  • |*Pandemics[MESH]
  • |*SARS-CoV-2[MESH]
  • |Acute Kidney Injury/*etiology/metabolism[MESH]
  • |COVID-19/complications/*epidemiology/metabolism[MESH]
  • |Chemokines/*metabolism[MESH]
  • |Humans[MESH]
  • |Kidney/*metabolism[MESH]


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