The co-occurrence of membranous nephropathy (MN) with MPO-ANCA related crescentic glomerulonephritis (MPO-rCGN) has been well described. Recent reports identified the myeloperoxidase (MPO) in membranous deposits in these cases, suggesting a role for MPO-ANCA in the pathogenesis of the membranous lesion in these patients. For the first time, we report a case of isolated MN (i.e. without concurrent MPO-rCGN) occurring in a patient with MPO-ANCA related arthritis, without MPO in membranous deposits. Case report A 69 year old male presented with a 5 month history of migratory polyarthralgias. Past history included localised prostate cancer and paroxysmal atrial fibrillation. ESR 69mm/hr. Haemoglobin 118 g/L. pANCA positive on immunofluorescence; MPO-ANCA titre 88 U/ml (normal < 20U/ml) on ELISA. Rheumatoid factor negative. ANA 1:80, with negative dsDNA and normal complement studies. Hepatitis B and C, and HIV serology negative. A diagnosis of MPO-ANCA related arthritis was made. He was noted to have microscopic haematuria (74 X 106 erythrocytes/L) and significant proteinuria – urinary protein excretion 5.5g/day. Renal function was normal – serum creatinine 75 umol/L, eGFR 89 ml/min/1.73m2. Serum albumin 29g/L. Blood pressure 127/74mmHg. No oedema. A renal biopsy demonstrated extensive basement membrane spikes along capillary loops, with intervening subepithelial deposits, consistent with stage 2 MN. Immunohistochemistry revealed moderate to strong capillary loop staining for IgG, IgG4, C3c and C1q. IHC staining with anti-MPO antibody was negative. PLA2R-antibody negative. Screening for malignancy revealed a new L1 vertebral lesion consistent with a metastasis from his known prostate cancer. Prednisolone 15mg daily was commenced which rapidly improved the joint symptoms and inflammatory markers. Methotrexate 10mg weekly was added 1 month later, and prednisolone weaned to 2.5mg over 6 months. Proteinuria improved rapidly, with protein excretion falling to 1.5g/day after 1 month of prednisolone. Complete remission of proteinuria occurred within 6 months. MPO-ANCA remained positive with no significant change in titre. Initial reports of concurrent MN and MPO-rCGN proposed that the lesions occurred together by chance. Recent reports have challenged this idea by demonstrating the presence of MPO in membranous deposits in these patients. Furthermore, the IgG subclasses in deposits have been shown to be IgG1 and IgG4, the subtypes which comprise most MPO-ANCA antibodies in the serum in ANCA vasculitis. It has thus been proposed that MPO/MPO-ANCA antibody complexes are pathogenic in forming the membranous deposits. The current case is the first report of isolated MN occurring in a patient with active MPO-ANCA related disease without concurrent MPO-rCGN. MPO was not identifiable in membranous deposits in this case, suggesting an alternative mechanism of injury. While it is possible the MN occurred secondary to prostate cancer, the strong IgG4 staining is atypical for malignancy associated MN. Additionally, the temporal relationship and parallel courses of activity of the MN and ANCA-related arthritis in response to treatment favours a pathogenetic link between the conditions. This case calls into question the role of MPO/MPO-ANCA antibody complexes in the pathogenesis of MN in patients with MPO-ANCA vasculitis.