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Primary peripheral PNET/Ewing's sarcoma of the dura with FISH analysis

deposits including C1q were found. Electron microscopy confirmed a moderate amount of electron-dense deposits in the mesangial and paramesangial regions (Figure 3). A diagnosis of IgA nephropathy with prominent crescent formation was made. With respect to the biopsy findings, the patient was put on intravenous methylprednisolone (500 mg for 3 days) and cyclophosphamide (50 mg daily) immunosuppressive therapy. There was no improvement in renal function and he died of septicaemia after 1 month. Autopsy was not performed. Nephrotic syndrome due to membranous glomerulonephritis has been well documented as one of the rare clinical manifestations of chronic GVHD. To the best of our knowledge only six cases of clinically significant GVHD-associated renal damage other than membranous nephropathy have been recorded in the English literature (Table 1). All these patients presented with heavy proteinuria ⁄ nephrotic syndrome. Minimal change disease, diagnosed in four of these patients, was the commonest form of glomerular injury. The pathogenesis of glomerular lesions after BMT is not well understood. It is generally believed that an immune complex-mediated mechanism during the course of GVHD may play a key role. Glomerular permeability might be altered by cytokines secreted by donor T lymphocytes in GVHD, thus accounting for the heavy proteinuria. IgA nephropathy was recognized in the setting of GVHD after BMT only recently. Mesangial deposition of Haemophilus parainfluenza outer membrane (OMHP) antigen and decrease in glycosylation of the IgA1 hinge have been implicated in the pathogenesis of IgA nephropathy. Such mechanisms have also been implicated in the aetiology of GVHD-associated IgA nephropathy after BMT. Recipient lymphocytes derived from donor haematopoietic stem cells may produce IgA-type antibody against OMHP antigen. The IgA might be damaged by infection or immunosuppressive therapy after BMT, become underglycosylated and deposited in the glomeruli. Though our patient had chronic HCV infection which has also been reported to be associated with IgA nephropathy, the relationship between HCV and IgA nephropathy is much debated and questionable. IgA nephropathy can complicate the course of GVHD after BMT. The clinical course of both Kimura et al’s and our case suggest an exacerbation associated with BMT and GVHD. IgA nephropathy should be entered into the differential diagnosis in patients who develop heavy proteinuria after BMT. G S-W Chan M F Lam W Y Au K C Tse T M Chan K N Lai K W Chan