Diao et al. [65] observed that kidney damage associated with COVID-19 is an acute tubular necrosis induced directly by SARS-CoV-2 during infection and replication, but also indirectly through the complex immune mechanisms triggered by cellular damage. In fact, the histopathological examination performed on kidney specimens, obtained from autopsy of COVID-19 patients with renal function impairment, showed viral antigens in the cytoplasm of the tubular cells, but also a strong presence of CD68+ macrophages in the tubulo-interstitium and strong C5b-9 depositions on the apical brush border of tubular epithelial cells (TECs). This suggested that proinflammatory cytokines derived from macrophages in the tubulo-interstitium and complement-mediated mechanisms resulting from cell damage participate in the pathogenesis of tubulo-interstitial damage. In fact, despite the infiltration of infected tissue by host immune cells in order to contain viral replication, the hyperactivation of these immune cells may lead to fibrosis, epithelial cell apoptosis and cause microvasculature damage [67,68,69].