#5132 POST-COVID-19 ANTI-GLOMERULAR BASEMENT MEMBRANE DISEASE: TWO CLINICAL CASES
Authors: Branco Carolina , Gameiro Joana , Oliveira João , Silva Bernardo Marques Da , Peres Nadiesda , Fonseca José Agapito , Fernandes Paulo , Godinho Iolanda , Outerelo Cristina , Jorge Sofia , Lopes José António , Nogueira Estela 
Published: June 2023

Background and Aims

Acute kidney injury is a common complication in patients hospitalized with COVID-19, has multiple aetiologies, and is usually multifactorial. We present two cases of anti-glomerular basement membrane (anti-GBM) disease diagnosed after SARS-CoV-2 infection, suggesting a causal correlation.

Case Reports

A 76-year-old female, with chronic kidney disease (serum creatinine 1.5mg/dL), hypertension, weight loss (16 Kg/6 months) and a pancreatic nodule under surveillance, presented to the emergency department with 1 week of nausea, vomits, diarrhoea and oliguria, as well as a history of mild SARS-CoV-2 infection 2 weeks before presentation. Lab work revealed severe anaemia (7.4 g/dL), inflammatory markers elevation, nephrotic proteinuria (proteinuria/creatininuria ratio 30 g/g), leucoerythrocyturia, serum creatinine of 19.3 mg/dL, hyperkalaemia and metabolic acidosis requiring dialysis induction. Renal ultrasound showed signs of chronicity and several cysts. Aetiological study disclosed positive anti-GBM antibody (1800 U/L) and negative ANCA. Complementary study failed to identify pulmonary involvement or neoplasms. Given the severity of the renal dysfunction along with the absence of alveolar haemorrhage, immunosuppression and plasmapheresis were not initiated. Patient was discharged and remains dialysis dependent. A 65-year-old male smoker with type 2 diabetes and combined pulmonary fibrosis and emphysema, presented in the emergency department with 2 months of asthenia, weight loss and anaemia, in addition to dyspnoea and haemoptysis in the past 3 days. Lab work exposed moderate anaemia (9.7 g/dL), elevated inflammatory markers, serum creatinine of 1.18 mg/dL (previously 0.8 mg/dL), leucoerythrocyturia and positive SARS-CoV-2 test. Angio-Computed Tomography exhibited known pulmonary fibrosis and possible bacterial superinfection. Despite antibiotic therapy (10 days of levofloxacin), haemoptysis remained and kidney function continuously worsened (serum creatinine 2.1 mg/dL). Complementary study showed positive ANCA-MPO (1125.4 U/L) and anti-GBM antibody (460.8U/L). Renal ultrasound was innocent. Kidney biopsy revealed: 6 glomeruli with cellular crescents with segmental necrosis, 3 with focal Bowman's capsule rupture; erythrocyte casts; intimal arterial fibrosis; moderate tubular atrophy; diffuse linear deposits of IgG. Immunosuppression was initiated with prednisolone (1 mg/Kg/day), cyclophosphamide (3x 12.5mg/Kg-750 mg, 2x 500 mg), rituximab (2x 1g), immunoglobulin (1x 2 g/Kg) and plasmapheresis (15 sessions). Kidney function continued to deteriorate (maximum serum urea 306 mg/dL, maximum serum creatinine 6.92 mg/dL) requiring dialysis induction 3 weeks after the beginning of immunosuppression. Even though haemoptysis ceased, the patient remains dialysis dependent 8 months after.

Conclusion

Literature reports an increase of Anti-GBM disease since the beginning of the pandemic. The presented cases support the apparent correlation, suggesting SARS-CoV-2 as a precipitant of this disease by endothelial injury with basal membrane exposure and autoantibody development. In the second case, the authors assume a subacute ANCA-MPO vasculitis with superimposed anti-GBM (eventually precipitated by COVID-19). Even though the causal association is not established, we highlight the importance of clinical suspicion of this rare aetiology in cases of acute kidney injury after SARS-CoV-2 infection.