A Rare Case of SARS-CoV-2-Induced Microscopic Polyangiitis

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection triggers elevated levels of circulating cytokines and immune-cell hyperactivation, called a cytokine storm, which leads to dysregulated immune response not only towards the pathogen itself but also contributes to cellular, vascular injury and multiorgan dysfunction. The cytokine-induced endothelial inflammation and vascular pathology of COVID-19 is well reported in post-mortem biopsies and several cases reporting small, medium and large vessel micro/macro thrombotic events and vasculitis in multiple organs. So far, few cases have been reported with newly diagnosed antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis at the time of acute COVID-19 infection. The exact pathophysiology of SARS-CoV-2 and ANCA-associated vasculitis continues to be studied and reviewed. Here we report a case of a 60-year-old female who presented to our institution with sudden onset of shortness of breath and hemoptysis. A detailed history revealed a recent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Labs showed elevated serum creatinine, urine analysis with large blood and nephrotic range proteinuria. CT chest was remarkable for abnormal appearance of the parenchyma bilaterally compatible with a crazy paving pattern, suggesting pulmonary alveolar proteinosis versus diffuse alveolar hemorrhage. Vasculitis was suspected and the patient was started on IV corticosteroids and plasmapheresis. Diagnostic workup was positive for antineutrophil cytoplasmic antibodies-myeloperoxidase (ANCA-MPO), anti-Sjögren's syndrome-related antigen A autoantibodies (anti-SS-A) and antinuclear antibodies (ANA). Renal biopsy confirmed focal segmental necrotizing, crescentic and sclerosing glomerulonephritis, pauci-immune type, anti-MPO antibody/P-ANCA associated. A diagnosis of microscopic polyangiitis was made and she was started on rituximab immunosuppressive therapy following which she showed clinical improvement. In this document, we present a unique case of microscopic polyangiitis possibly induced by SARS-CoV-2 infection confirmed by renal biopsy and clinical presentation. In the current setting of a global pandemic, we strongly recommend that vasculitis be high on the differential diagnosis in patients who are currently infected or had been infected with SARS-CoV-2 and present with acute kidney injury (AKI).

Possible Association Between COVID-19 Infection and De Novo Antineutrophil Cytoplasmic Antibody-Associated Vasculitis

“…To date, only a handful cases of possible association between COVID-19 and AAV have been reported. Patients have presented with either glomerulonephritis (GN), DAH, or both, during or shortly after COVID-19 [4][5][6][7][8][9][10][11]. This is a case report of a rare AAV presenting with pulmonary-renal syndrome in the immediate post infectious recovery.…”

“…Lately, case reports have suggested an association between COVID-19, immune system dysregulation and cytokine storm. De novo presentation of anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis during COVID-19 has been recently reported in a few cases [4][5][6][7][8][9][10][11]. Patients presented with either AKI, diffuse alveolar hemorrhage (DAH), or both.…”

Vasculitis flare after COVID-19: report of two cases in patients with preexistent controlled IgA vasculitis and review of the literature

“…We identified 16 reports describing 18 cases (12 women/6 men) of new-onset ANCA-associated vasculitis in COVID-19 patients and presumably related to this disease [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. The main characteristics of these cases are presented in Table 1.…”

Propylthiouracil-Induced Antineutrophil Cytoplasmic Antibody-Associated Vasculitis after COVID-19 Vaccination

“…There are several reports of new-onset AAV following COVID-19 [ 18 , 19 , 20 ]. Direct endothelial injury by the virus, complement activation, and activation of neutrophils resulting in the formation of neutrophil extracellular traps (NETs) may drive the development of AAV [ 21 , 22 ].…”