The pathophysiology of AKI associated with COVID-19 could be related not only to non-specific mechanisms but also to COVID-specific mechanisms, such as direct cell injury caused by SARS-CoV-2 entry through the receptor (ACE2), which is highly expressed in the kidney, imbalance of the renin–angiotensin–aldosterone system, and pro-inflammatory cytokines caused by the SARS-CoV-2 infection and thrombotic events (Gabarre et al., 2020). Here, ACE2 is linked to acute kidney injury.