Abstract
Patients affected by severe COVID-19 infection often develop end-organ damage that manifests as acute kidney injury (AKI).1,2 It has been reported that greater than 20% of such patients are diagnosed with AKI, but the long term impact on future prevalence of chronic kidney disease has yet to be rigorously quantitated.3 There is substantial evidence that primary events of AKI in this circumstance occur on the luminal surface of the endothelial cell in the microvasculature of the kidney,4-7 including histopathological descriptions of kidney-specific endothelitis and glomerular fibrin thrombi.
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