Renal Considerations in COVID-19: Biology, Pathology, and Pathophysiology

Kapp, Meghan E.; Fogo, Agnes B.; Roufouse, Candice; Najafian, Behzad; Radhakrishnan, Jai; Mohan, Sumit; Miller, Sara E.; D’Agati, Vivette D.; Silberzweig, Jeffrey; Barbar, Tarek; Gopalan, Tulasi; Srivatana, Vesh; Mokrzycki, Michele H.; Benstein, Judith A.; Ng, Yue-Harn; Lentine, Krista L.; Aggarwal, Vikram; Perl, Jeffrey; Salenger, Page; Koyner, Jay L.; Josephson, Michelle A.; Heung, Michael; Velez, Juan Carlos; Ikizler, Alp; Vijayan, Anitha; William, Preethi; Thajudeen, Bijin; Slepian, Marvin J.

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.