Kidney involvement is rapidly emergingasaprominentpartof the clinical spectrum of coronavirus disease 2019 (COVID-19) and is associated with mortality. 1 Given that the angiotensin-converting enzyme 2 receptor, which is the cellular entry point for severe acute respiratory syndrome coronavirus 2, is expressed on podocytes, renal tubular epithelial cells, and endo- thelial cells, direct viral tissue dam- age is a plausible mechanism of kidney injury. 2 In addition, dysre- gulation of immune responses, microvascular thrombosis, hypo- volemia, use of mechanical ventila- tion, hemodynamic instability, collapsing glomerulopathy, organo- tropism, and maladaptation of angiotensin-converting enzyme 2– related pathways have all been implicatedinglomerulardiseaseand acute tubular damage in the context of COVID-19.
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