Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China

Acute Kidney Injury in COVID-19: Emerging Evidence of a Distinct Pathophysiology

“…An important report on autopsy findings from deceased patients with COVID-19 again demonstrated prominent acute proximal tubular injury, but also peritubular erythrocyte aggregation and glomerular fibrin thrombi with ischemic collapse. 3 This paper also reported endothelial damage, hemosiderin deposition, pigment casts related to rhabdomyolysis, and inflammation. Notably, some of these patients lacked evidence of AKI as detected by routine measures (creatinine and/or BUN), highlighting the possibility of substantial subclinical kidney injury.…”

Hypertension, Thrombosis, Kidney Failure, and Diabetes: Is COVID-19 an Endothelial Disease? A Comprehensive Evaluation of Clinical and Basic Evidence

“…According to immunohistochemistry assays [140], ACE2 seems not to be expressed in renal endothelial cells; however, a study based on single-cell analysis has confirmed the expression of ACE2 and TMPRSS2 in human renal endothelial cells [141], and most recently the presence of viral particles was confirmed by electron microscopy in endothelial cells of the glomerular capillary loops of a COVID-19 patient [142]. Besides, endothelial damage was a common finding in renal histopathological analyses of 26 COVID-19 patients, in the absence of interstitial inflammatory infiltrates [143].…”

COVID-19 — Toward a comprehensive understanding of the disease

“…However, renal podocytes and proximal tubule cells express both of the viral receptors -ACE2 and TMPRSS2, serving as a target for it [12,23]. Virus particles were identified in podocytes and proximal tubular epithelium on autopsy [95]. Prominent acute proximal tubule injury was observed, which manifested itself as the loss of brush border, vacuolar degeneration, dilatation of the tubular lumen with cellular debris, and occasionally even frank necrosis and detachment of epithelium with the bared tubular basement membrane [95].…”

“…Virus particles were identified in podocytes and proximal tubular epithelium on autopsy [95]. Prominent acute proximal tubule injury was observed, which manifested itself as the loss of brush border, vacuolar degeneration, dilatation of the tubular lumen with cellular debris, and occasionally even frank necrosis and detachment of epithelium with the bared tubular basement membrane [95]. Glomerular thrombosis, fibrin sediments or platelet aggregates were not observed, suggesting that local thrombosis had not been triggered [95].…”

“…Prominent acute proximal tubule injury was observed, which manifested itself as the loss of brush border, vacuolar degeneration, dilatation of the tubular lumen with cellular debris, and occasionally even frank necrosis and detachment of epithelium with the bared tubular basement membrane [95]. Glomerular thrombosis, fibrin sediments or platelet aggregates were not observed, suggesting that local thrombosis had not been triggered [95]. Intensivists from the United Kingdom suggested a careful water balance assessment in patients with COVID-19 ARDS on admission to ICU, as apart from the heavy lung injury, they frequently presented with dehydration and even hypovolemia.…”