Acute kidney injury in SARS-CoV-2 infected patients

Fanelli, Vito; Fiorentino, Marco; Cantaluppi, Vincenzo; Gesualdo, Loreto; Stallone, Giovanni; Ronco, Claudio; Castellano, Giuseppe

AKI represents a life-threatening complication in critically ill patients, often leading to increased risk of death. As recently reported by Wilson et al., the onset of moderate-to-severe AKI described a higher-risk subset of ARDS patients, with a significant risk for mortality [4] . Considering the possible pathogenic mechanisms of AKI-associated ARDS, AKI may be ascribed to different causes such as impairment of gas exchange, hemodynamic alterations including right heart failure, fluid overload and systemic congestion, injurious mechanic ventilation strategies, and development of secondary infections/sepsis. Several studies emphasized the relevance of the inflammatory/immune-mediated reaction with the release of high levels of circulating harmful mediators capable to interact with kidney-resident cells causing endothelial dysfunction, microcirculatory derangement, and tubular injury [5] . In accordance with previous studies, the beta coronaviruses SARS-CoV and the most recent SARS-CoV-2 use angiotensinconverting enzyme 2 (ACE-2) as receptor to facilitate viral entry into target cells; ACE-2 is also located on the surface of kidney tubular cells, and their infection may worsen the local inflammatory response and consequently the incidence and the duration of AKI episodes [6] (Table 1) .