Although the respiratory and immune systems are the major targets of
Coronavirus Disease 2019 (COVID-19),
acute kidney injury and
proteinuria have also been observed. Currently, detailed pathologic examination of kidney damage in
critically ill patients with
COVID-19 has been lacking. To help define this we analyzed kidney abnormalities in 26 autopsies of patients with
COVID-19 by light microscopy, ultrastructural observation and immunostaining. Patients were on average 69 years (19 male and 7 female) with
respiratory failure associated with
multiple organ dysfunction syndrome as the cause of death. Nine of the 26 showed clinical signs of kidney injury that included increased serum
creatinine and/or new-onset
proteinuria. By light microscopy, diffuse proximal tubule injury with the loss of brush border, non-isometric vacuolar degeneration, and even frank
necrosis was observed. Occasional
hemosiderin granules and pigmented casts were identified. There were prominent erythrocyte aggregates obstructing the lumen of capillaries without platelet or fibrinoid material. Evidence of
vasculitis, interstitial
inflammation or
hemorrhage was absent. Electron microscopic examination showed clusters of coronavirus-like particles with distinctive spikes in the tubular epithelium and podocytes. Furthermore, the receptor of SARS-CoV-2, ACE2 was found to be upregulated in patients with
COVID-19, and immunostaining with SARS-CoV
nucleoprotein antibody was positive in tubules. In addition to the direct virulence of SARS-CoV-2, factors contributing to
acute kidney injury included systemic
hypoxia, abnormal coagulation, and possible drug or
hyperventilation-relevant
rhabdomyolysis. Thus, our studies provide direct evidence of the invasion of SARSCoV-2 into kidney tissue. These findings will greatly add to the current understanding of
SARS-CoV-2 infection.