Renal Considerations in COVID-19: Biology, Pathology, and Pathophysiology.
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has emerged into a worldwide pandemic of epic proportion. Beyond pulmonary involvement in coronavirus disease 2019 (COVID-19), a significant subset of patients experiences acute kidney injury. Patients who die from severe disease most notably show diffuse acute tubular injury on postmortem examination with a possible contribution of focal macro- and microvascular thrombi. Renal biopsies in patients with proteinuria and hematuria have demonstrated a glomerular dominant pattern of injury, most notably a collapsing glomerulopathy reminiscent of findings seen in human immunodeficiency virus (HIV) in individuals with apolipoprotein L-1 (APOL1) risk allele variants. Although various mechanisms have been proposed for the pathogenesis of acute kidney injury in SARS-CoV-2 infection, direct renal cell infection has not been definitively demonstrated and our understanding of the spectrum of renal involvement remains incomplete. Herein we discuss the biology, pathology, and pathogenesis of SARS-CoV-2 infection and associated renal involvement. We discuss the molecular biology, risk factors, and pathophysiology of renal injury associated with SARS-CoV-2 infection. We highlight the characteristics of specific renal pathologies based on native kidney biopsy and autopsy. Additionally, a brief discussion on ancillary studies and challenges in the diagnosis of SARS-CoV-2 is presented.
Kapp, ME; Fogo, AB; Roufouse, C; Najafian, B; Radhakrishnan, J; Mohan, S; Miller, SE; D'Agati, VD; Silberzweig, J; Barbar, T; Gopalan, T; Srivatana, V; Mokrzycki, MH; Benstein, JA; Ng, Y-H; Lentine, KL; Aggarwal, V; Perl, J; Salenger, P; Koyner, JL; Josephson, MA; Heung, M; Velez, JC; Ikizler, A; Vijayan, A; William, P; Thajudeen, B; Slepian, MJ
Volume / Issue
Start / End Page
Pubmed Central ID
Electronic International Standard Serial Number (EISSN)
Digital Object Identifier (DOI)