Abstract
Acute kidney injury is a frequent complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), principally because of hypotension and decreased kidney perfusion secondary to haemodynamic or haemostatic factors, drug-induced nephrotoxicity, and cytokine storm syndrome related to sepsis. Additionally, several factors support the existence of SARS-CoV-2-associated nephropathy, such as early, new-onset proteinuria and haematuria in many patients, the identification of SARS-CoV-2 viral load in precisely defined kidney compartments, ultrastructural and immunohistochemical evidence of direct viral infection of the kidneys, and, most importantly, morphological alterations associated with cytopathic action induced by the virus. In addition, collapsing glomerulopathy that has been reported in patients of African American descent with underlying apolipoprotein L1 (APOL1) kidney risk alleles and SARS-CoV-2 infection is evidence of a distinct form of SARS-CoV-2-associated nephropathy, the APOL1-SARS-CoV2-associated nephropathy.
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