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D-penicillamine is an effective disease-modifying drug in rheumatoid arthritis, but adverse effects are common and often lead to the cessation of treatment with this agent [1]. A variety of autoimmune disorders may be induced by the drug, either associated with organspecific autoantibodies (e.g. myasthenia gravis or pemphigus vulgaris) or with non-organ-specific autoantibodies (e.g. systemic lupus erythematosus) [2,3]. Renal injury is seen in up to 30% of patients treated with peniciUamine, typically causing proteinuria without impairment of renal excretory capacity [4]. The commonest histological finding is membranous nephropathy, but in a minority of cases there will be minimalchange nephropathy or the presence of electron-dense mesangial deposits [4].

Coexistent membranous nephropathy and ANCA-positive crescentic glomerulonephritis in association with penicillamine