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COVID-19 and acute kidney injury

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dc.creator Kanbay, Asiye
dc.creator Kanbay, Mehmet
dc.creator ELSÜRER AFŞAR, Rengin
dc.creator AFŞAR, Barış
dc.creator Ertuglu, Lale A.
dc.date 2020-01-01T00:00:00Z
dc.date.accessioned 2021-12-03T12:05:09Z
dc.date.available 2021-12-03T12:05:09Z
dc.identifier f4b79ea5-b4be-4f8d-bd1a-a6fc75dfa1a9
dc.identifier 10.5578/tt.70010
dc.identifier https://avesis.sdu.edu.tr/publication/details/f4b79ea5-b4be-4f8d-bd1a-a6fc75dfa1a9/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/95839
dc.description The Coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) started in December 2019 and has affected millions of lives worldwide, while many aspects of the illness are still unknown. Current data show that many hospitalized COVID-19 patients suffer from kidney damage, in the form of proteinuria, hematuria or acute kidney injury (AKI). AKI is especially prevalent among severe and critically ill COVID-19 patients and is a predictor of mortality. The pathophysiology of AKI in COVID-19 is unclear. Early reports of histopathologic examination from autopsied kidney tissue show SARS-CoV-2 viral particles in renal tubular cells and podocytes, suggesting direct viral infection, as well as findings of acute tubular necrosis, while rhabdomyolysis-associated AKI and glomerulopathies may also occur. As of today, only remdesivir has been authorized to treat COVID-19. Ongoing research investigates potential of anti-viral and anti-inflammatory agents along with safety and efficacy of commonly prescribed drugs such as renin-angiotensin-aldosterone system blockers. This review discusses the prevalence of AKI and its association with outcome, while highlighting possible mechanisms of AKI and suggesting organ protective measures to prevent the development of kidney damage.
dc.language eng
dc.rights info:eu-repo/semantics/openAccess
dc.title COVID-19 and acute kidney injury
dc.type info:eu-repo/semantics/article


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