4.5 Review

Is the kidney a target of SARS-CoV-2?

Journal

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Volume 318, Issue 6, Pages F1454-F1462

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00160.2020

Keywords

acute kidney injury; angiotensin-converting enzyme 2; COVID-19; proteinuria; renin-angiotensin-aldosterone system

Funding

  1. Mexican Council of Science and Technology (CONACyT) [A1-S-8715]
  2. Universidad Nacional Autonoma de Mexico [IN201619]
  3. CONACYT [961986]

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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 SARSCoV-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.

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