| Literature DB >> 34191753 |
Meghan E Kapp1, Agnes B Fogo, Candice Roufouse, Behzad Najafian, Jai Radhakrishnan, Sumit Mohan, Sara E Miller, Vivette D D'Agati, Jeffrey Irs Silberzweig, Tarek Barbar, Tulasi Gopalan, Vesh Srivatana, Michele H Mokrzycki, Judith A Benstein, Yue-Harn Ng, Krista L Lentine, Vikram Aggarwal, Jeffrey Perl, Page Salenger, Jay Coyner, Michelle A Josephson, Michael Heung, Juan Carlos Velez, Alp Ikizler, Anitha Vijayan, Preethi William, Bijin Thajudeen, Marvin J Slepian.
Abstract
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has emerged into a worldwide pandemic of epic proportion. Beyond pulmonary involvement in 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 HIV in individuals with apolipoprotein L-1 (APOL-1) 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.Entities:
Year: 2021 PMID: 34191753 DOI: 10.1097/MAT.0000000000001530
Source DB: PubMed Journal: ASAIO J ISSN: 1058-2916 Impact factor: 2.872