Abstract
BackgroundAnti-glomerular basement membrane disease (GBM) disease is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage. Recently, an association between COVID-19 and anti-glomerular basement membrane (anti-GBM) disease has been proposed. We report on a patient with recurrence of anti-GBM disease after SARS-CoV-2 infection.Case presentationThe 31-year-old woman had a past medical history of anti-GBM disease, first diagnosed 11 years ago, and a first relapse 5 years ago. She was admitted with severe dyspnoea, haemoptysis, pulmonary infiltrates and acute on chronic kidney injury. A SARS-CoV-2 PCR was positive with a high cycle threshold. Anti-GBM autoantibodies were undetectable. A kidney biopsy revealed necrotising crescentic glomerulonephritis with linear deposits of IgG, IgM and C3 along the glomerular basement membrane, confirming a recurrence of anti-GBM disease. She was treated with steroids, plasma exchange and two doses of rituximab. Pulmonary disease resolved, but the patient remained dialysis-dependent. We propose that pulmonary involvement of COVID-19 caused exposure of alveolar basement membranes leading to the production of high avidity autoantibodies by long-lived plasma cells, resulting in severe pulmonary renal syndrome.ConclusionOur case supports the assumption of a possible association between COVID-19 and anti-GBM disease.
Highlights
BackgroundAnti-glomerular basement disease (anti-glomerular basement membrane disease (GBM) disease) is a rare small-vessel vasculitis
Anti-glomerular basement membrane disease (GBM) disease is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage
Our case supports the assumption of a possible association between COVID-19 and anti-GBM disease
Summary
Anti-glomerular basement disease (anti-GBM disease) is a rare small-vessel vasculitis. GBM antibodies were detected (titre 137 U/ml), and a renal biopsy showed linear IgG deposits along the glomerular basement membrane. She was treated with 1 g iv prednisolone for 3 days followed by 80 mg orally, plasma exchange, and six cycles of iv cyclophosphamide 750 mg. After an allergic reaction to fresh frozen plasma, therapy was switched from plasma exchange to immunoadsorption using Ig-Therasorb® columns with Sepharose-coupled polyclonal sheep antibodies against human immunoglobulins She responded clinically well to treatment and anti-GBM antibodies became negative. A test for anti-GBM antibodies was borderline (titre 20 U/mL) She was treated with 500 mg iv prednisolone for 3 days followed by 80 mg orally, plasma exchange and two 1-g doses of rituximab.
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