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10.1152/ajprenal.00160.2020

http://scihub22266oqcxt.onion/10.1152/ajprenal.00160.2020
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32412303!7303722!32412303
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suck abstract from ncbi

pmid32412303      Am+J+Physiol+Renal+Physiol 2020 ; 318 (6): F1454-F1462
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  • Is the kidney a target of SARS-CoV-2? #MMPMID32412303
  • Martinez-Rojas MA; Vega-Vega O; Bobadilla NA
  • Am J Physiol Renal Physiol 2020[Jun]; 318 (6): F1454-F1462 PMID32412303show ga
  • The new disease produced by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) represents a major pandemic event nowadays. Since its origin in China in December 2019, there is compelling evidence that novel SARS-CoV-2 is a highly transmissible virus, and it is associated to a broad clinical spectrum going from subclinical presentation to severe respiratory distress and multiorgan failure. Like other coronaviruses, SARS-CoV-2 recognizes human angiotensin-converting enzyme 2 as a cellular receptor that allows it to infect different host cells and likely disrupts renin-angiotensin-aldosterone system homeostasis. Particularly, a considerable incidence of many renal abnormalities associated to COVID-19 has been reported, including proteinuria, hematuria, and acute kidney injury. Moreover, it has been recently demonstrated that SARS-CoV-2 can infect podocytes and tubular epithelial cells, which could contribute to the development of the aforementioned renal abnormalities. In this review, we discuss the biological aspects of SARS-CoV-2 infection, how understanding current knowledge about SARS-CoV-2 infection may partly explain the involvement of the kidneys in the pathophysiology of COVID-19, and what questions have arisen and remain to be explored.
  • |*Betacoronavirus[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*complications/metabolism[MESH]
  • |Humans[MESH]
  • |Kidney Diseases/*virology[MESH]
  • |Kidney/*virology[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/metabolism[MESH]
  • |Pneumonia, Viral/*complications/metabolism[MESH]


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