To the editor:

The diagnosis and management of autoimmune disorders is challenging in the current pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here, we describe the case of a patient with anti–glomerular basement membrane (GBM) disease complicated by a SARS-CoV-2 infection to highlight the importance of appropriate immunosuppression and individualized care in respect of these 2 disease processes.

The 44-year-old Caucasian male presented to the emergency department with palpitations and a new tickling cough. He displayed tachycardia, lymphopenia (0.21 × 10⁹/L), and a positive rapid test for SARS-CoV-2. He recently had been diagnosed with anti-GBM glomerulonephritis (GN), causing an acute kidney injury. He was receiving alternate-day plasma exchange, oral glucocorticoids, and i.v. cyclophosphamide pulses to preserve kidney function. His chest radiography did not reveal any pneumonic consolidation. He was admitted to the hospital and commenced on remdesivir. He did not develop more severe symptoms of pneumonitis typical for SARS-CoV-2. After 5 days of remdesivir treatment, he was discharged and his plasma exchange and cyclophosphamide therapies were restarted while he remained SARS-CoV-2 polymerase chain reaction (PCR)–positive. SARS-CoV-2 PCR became undetectable after a total of 31 days, and SARS-CoV-2 antibodies were detected (Figure 1 ).

Figure 1

Induction immunotherapy for anti–glomerular basement membrane (GBM) disease complicated by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patient received plasma exchange (PLEX) and i.v. cyclophosphamide (CyP) pulse therapy and oral prednisolone. Depicted are his GBM antibody level (U/L), renal function (creatinine in μmol/L), lymphocyte count (×10⁹/L), SARS-CoV-2 quantitative polymerase chain reaction (PCR) in million viral copies/swab, and antibody (AB) levels (ratio/index).

The current pandemic is a global health threat and a great challenge to vasculitis and GN care. Here, we describe a SARS-CoV-2 infection in a vasculitis patient in which the viral infection remained mild despite aggressive immunotherapy. A registry of SARS-CoV-2 infection in patients with immune-mediated kidney diseases proposed a higher mortality in GN patients.¹ Waldman et al. detected a higher rate of acute kidney injury and a more pronounced hypoalbuminaemia in 40 GN patients as potential causes for the adverse outcome, while the immunotherapy did not correlate with mortality. Risk stratification in SARS-CoV-2 disease is evolving.2, 3, 4 SARS-CoV-2 vaccination will be the most important step toward protecting immune-compromised patients. In the presence of scarce resources, equitable and effective risk–benefit allocation will be vital, prioritizing vulnerable patients. Timing immunotherapy with vaccination and determining vaccination response will be crucial. Concurrent SARS-CoV-2 infection should not prevent delivery of effective immunomodulatory therapy in patients with severe autoimmune diseases, essential for the protection and recovery of vital organ function.