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Background

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the pathogen responsible of atypical pneumonia that has affected more than 330,000 people and caused death of more than 14,000 patients (as of March 23, 2020, WHO Report). Coronavirus spike (S) glycoproteins mediate entry into cells end predominantly lung epithelial alveolar cells precipitating an interstitial pneumonia that evolves through acute respiratory distress syndrome (ARDS)[1]. Interestingly, about 25% of acute kidney injury (AKI) occurrence has been reported in this clinical setting [2, 3]. These data were recently confirmed by the Italian Report of “Istituto Superiore di Sanità” describing an incidence of 27.8% in more than 2000 patients (updated on 17 March)(https://www. epicentro. iss. it/coronavirus/bollettino/Report-COVID-2019_17_marzo-v2. pdf). In this commentary, we discuss possible mechanisms of the COVID-19 …