Untitled

Abstract

CoMMentARy of RNA beta-coronavirus, which include the virus that were responsible for the outbreaks of severe acute respiratory syndrome (SARS) and middle east respiratory syndrome (MERS) between 2012 and 2013 [3,4]. COVID-19 has a variable mortality rate according to each country and is expected to affect a major part of the world's population [2]. The clinical spectrum of COVID-19 infection is variable, ranging from asymptomatic carrier state, anosmia, ageusia or minor upper respiratory tract illness to severe pneumonia potentially leading to acute respiratory distress syndrome (ARDS), respiratory failure, multiple organ disfunction and even death [5]. Diarrhea and cutaneous and thrombotic manifestations were recently described [6]. SARS-CoV-2 mainly affects the respiratory system causing acute respiratory illness, with bilateral and diffuse pneumonia, but it can affect multiple organs and systems, such as the kidneys [6]. Kidney cells express receptors and enzymes required for viral entry, such as angiotensin-converting enzyme 2 (ACE2), which is also expressed in the lung, heart and intestine [7,8]. Furthermore, kidney damage may result from hemodynamic factors or dysfunctional immune response. Direct renal cell infection is possible and is supported by some studies showing viral particles within proximal tubules and podocytes [9], as indicated by presence of proteinuria and hematuria. Inflammatory cytokines have long been known to induce acute kidney injury (AKI), glomerulopathy [10], and a spectrum of