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Am J Case Rep . Diagnosis of Dual c- and p-ANCA Vasculitis Following SARS-CoV-2 Infection: A Case Report

tetano

Editor, Senior Moderator
Am J Case Rep


. 2026 Jan 19:27:e950958.
doi: 10.12659/AJCR.950958.
Diagnosis of Dual c- and p-ANCA Vasculitis Following SARS-CoV-2 Infection: A Case Report

Isaac B Wolfkind[SUP] 1 [/SUP], Ronan J McOsker[SUP] 1 [/SUP], Debra Karling[SUP] 1 [/SUP], Connor McKinney[SUP] 2 [/SUP], Eslam Mohamed[SUP] 1 3 [/SUP]


Affiliations
Abstract

BACKGROUND Anti-neutrophil cytoplasmic antibodies (ANCAs) are associated with a group of small-vessel vasculitides collectively known as ANCA-associated vasculitis (AAV), which can lead to rapidly progressive glomerulonephritis and multisystem involvement. In addition to other autoimmune diseases, AAV has been increasingly reported following SARS-CoV-2 infection. CASE REPORT We present the case of a 70-year-old woman with a past medical history of atrial fibrillation, sick sinus syndrome, breast cancer, gastroesophageal reflux disease, and anxiety, who developed a rare phenomenon of dual ANCA-positive pauci-immune glomerulonephritis following coronavirus disease 2019 (COVID-19). She initially presented with refractory sinusitis and a persistent cough. Over 5 months, she developed iron-deficiency anemia and, eventually, a rapid decline in renal function. Serologic testing revealed dual positivity for anti-proteinase 3 (PR3, c-ANCA) and anti-myeloperoxidase (MPO, p-ANCA). Renal biopsy confirmed pauci-immune glomerulonephritis. She was ultimately diagnosed with granulomatosis with polyangiitis (GPA). CONCLUSIONS This case highlights a potential post-infectious autoimmune phenomenon triggered by SARS-CoV-2 and underscores the importance of considering AAV in patients with unexplained systemic symptoms and renal dysfunction after COVID-19. Furthermore, the mechanism of AAV seroconversion and disease progression may be linked to the ability of SARS-CoV-2 to induce the formation of neutrophil extracellular traps (NETs) through both direct viral-neutrophil interactions and cytokine-mediated inflammation. Our findings contribute to the growing body of evidence linking viral infections to the emergence of autoimmune vasculitis.


 
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