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Published on: February 2, 2021
Glomerular Endotheliosis in COVID-19-Associated Acute Kidney Injury
Barbara Garay1, Deep Phachu2, Srimathi Manickaratnam2
1Internal Medicine, University of Connecticut Health, Farmington, USA.
Insights
This case study highlights a patient with lupus nephritis who developed acute kidney injury due to SARS-CoV-2 (COVID-19) infection. The study suggests COVID-19 may trigger anti-angiogenic factors, leading to glomerular endotheliosis and renal failure.
Area of Science:
- Nephrology
- Infectious Diseases
- Pathophysiology
Background:
- Acute kidney injury (AKI) is a known complication in patients with SARS-CoV-2 (COVID-19) infection.
- The exact mechanisms of glomerular injury in COVID-19 remain unclear.
- Lupus nephritis patients in remission may be susceptible to novel kidney injury pathways.
Abstract:
Acute kidney injury (AKI) has been seen in patients hospitalized with a SARS-CoV-2 (COVID-19) infection,but the pathophysiology of glomerular injury is not yet fully understood. We present a case of COVID-19-related "glomerular endotheliosis" in which a 51-year-old female with a 13-year history of class IV lupus nephritis was admitted for COVID-19 pneumonia. Her lupus nephritis had been in complete renal remission for the past 10 years with a baseline serum creatinine level of 1.3 mg/dL and no proteinuria. Her serological workup, including complement levels, was unremarkable. Due to the worsening renal function and persistent proteinuria, she underwent a kidney biopsy that revealed diffuse glomerular endothelial cell swelling, also known as glomerular endotheliosis. Her clinical course unfortunately deteriorated and she succumbed to acute respiratory distress syndrome. As circulating anti-angiogenic factors may contribute to the pathogenesis of endothelial dysfunction leading to glomerular endotheliosis, we propose that a similar circulating antiangiogenic factor may have been triggered by COVID-19 and played a role in our patient's progressive renal failure.
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