SYSTEMATIC REVIEW article
Front. Med.
Sec. Nephrology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1568943
This article is part of the Research TopicChallenge to the Future: Advances in post-COVID-19 intensive care NephrologyView all 4 articles
Ascertaining the mechanistic etiology of COVID-associated glomerulonephritis: a systematic review
Provisionally accepted
Brendan Coyne1*
Danielle Ito2Anam Tariq1
Susie Lew1Jeffrey Kopp3Fahim Malik4
Patrick Gipson1*Ehsan Nobakht1- 1George Washington University Hospital, Washington, D.C., United States
- 2University of California, Irvine, Irvine, California, United States
- 3National Institute of Diabetes and Digestive and Kidney Diseases (NIH), Bethesda, Maryland, United States
- 4Washington Nephrology Associates, Rockville, United States
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Since its first reported case in December 2019, COVID-19 disease, caused by severe acute respiratory coronavirus 2 (SARS-CoV-2), evolved into a major pandemic throughout the world. Although COVID-19 is most often characterized as a respiratory pathology, there are also extensive reports of renal complications, such as glomerulonephritis (GN). However, the precise nature of COVID-associated glomerulonephritis (COVID-GN) has yet to be fully understood. This review seeks to elucidate COVID-GN pathophysiology by conducting an exhaustive systematic review. Herein, we compare the different GN subtypes associated with COVID-19 in the literature. We also the cytokines, antibodies, and genes most implicated in COVID-GN. The GN subtype with the highest number of cases associated with COVID-19 infection was focal segmental glomerulosclerosis, specifically the collapsing morphology. Meanwhile, the highest number of cases associated with COVID-19 vaccination was IgA nephropathy. The most prevalent mechanism in the literature for COVID-GN involves a cytokine storm, which may be accompanied by immune complex deposition. Both infection and vaccination from SARS-CoV-2 can induce robust CD4+ T cell responses promoted by an IL-6 amplifier loop of inflammation. This immune response is likely further enhanced by interactions with complement systems and the renin-angiotensin-aldosterone system (RAAS). SARS-CoV-2-mediated pathways of both direct cytotoxicity and stimulation of polyclonal immunoglobulin may converge to cause glomerular inflammation and injury. Further investigation of these inflammatory pathways may provide insight in COVID-19 pathophysiology, treatment, and long-term outcomes.
Keywords: COVID-19, Glomerulonephritis, glomerulopathies, COVID-19 associated nephropathy, immunology, immune complex, Cytokines, Vaccines 2.2 Data Extraction
Received: 31 Jan 2025; Accepted: 14 May 2025.
Copyright: © 2025 Coyne, Ito, Tariq, Lew, Kopp, Malik, Gipson and Nobakht. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Brendan Coyne, George Washington University Hospital, Washington, D.C., United States
Patrick Gipson, George Washington University Hospital, Washington, D.C., United States
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