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

Abstract

The new disease produced by the 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 multi-organ failure. Like other coronaviruses, SARS-CoV-2 recognizes the human Angiotensin Converting Enzyme 2 (hACE2) as a cellular receptor that allows it to infect different host cells, and likely disrupts the renin-angiotensin-aldosterone system (RAAS) homeostasis. Particularly, it has been reported a considerable incidence of many renal abnormalities associated to COVID-19, including proteinuria, hematuria and acute kidney injury (AKI). 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 the 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 arise and remain to be explored.