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Anti-glomerular basement membrane-antibody disease in a patient treated with adalimumab for rheumatoid arthritis

Ttumour necrosis factor-alpha (TNF-α) blockade has been linked to the induction of autoimmunity, including autoimmune renal disorders. To our knowledge, there have been no cases of anti-TNF-α therapy associated with anti-glomerular basement membrane (GBM)-antibody disease reported. A 63-year-old male presented with anuric acute renal failure and was found to have a rapidly progressive glomerulonephritis secondary to anti-GBM-antibody disease. This occurred in the setting of 4 years of adalimumab treatment for rheumatoid arthritis and normal baseline renal function. This was preceded by a gastrointestinal illness and nonsteroidal anti-inflammatory use. His anti-GBM titre was >1000 chemiluminescent units at presentation. A renal biopsy revealed a crescentic necrotising glomerulonephritis with linear staining of immunoglobulin G in the GBM. He was treated with pulse intravenous methylprednisolone and later changed to high-dose prednisolone and cyclophosphamide. Four weeks of plasma exchange was completed. He remains dialysis dependent. There is a known association between TNF-α blockade and occurrence of autoimmune renal diseases. Given the rarity of anti-GBM-antibody disease, it is plausible that there could be an association between treatment with adalimumab and anti-GBM-antibody disease., the present case highlights the ongoing need for monitoring of renal function, urinary sediment and proteinuria in patients exposed to these novel therapies.