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Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Case Presentation:
A 39-year-old Japanese man was admitted to a previous hospital for progressive leg edema and renal impairment (serum creatinine 1.83 mg/dL). Autoantibody screening was negative, but serum immunofixation revealed an IgM-κ monoclonal protein. Light microscopy showed lobulated glomeruli with extensive eosinophilic, PAS-positive deposits distributed in subendothelial, intracapillary, and mesangial areas (Figure A). By immunofluorescence, strong deposits of IgM, C3c, and κ light chain were observed in capillary wall and mesangial patterns. Electron microscopy shows marked subendothelial and intracapillary electron-dense deposits extensively involving the glomerular capillary loops and nearly occluding the lumina, with orderly-arranged microtubular ultrastructure approximately 20 nm in diameter (Figure B, C). PET-CT showed no significant lymphadenopathy. The initial diagnosis was light chain deposition disease associated with monoclonal gammopathy; however, as renal function rapidly deteriorated and nephrotic syndrome developed, the patient was referred to our hospital. On admission, blood pressure was 155/96 mmHg, with leg edema evident. Laboratory findings showed a urine protein/creatinine ratio of 4.37 g/gCr, hemoglobin 7.7 g/dL, serum albumin 2.4 g/dL, serum creatinine 5.16 mg/dL, IgM 222 mg/dL, and κ/λ ratio 4.89. Urinary Bence Jones protein and cryoglobulin were negative. Bone marrow biopsy detected a MYD88 mutation, leading to a diagnosis of lymphoplasmacytic lymphoma(LPL). Although DRC therapy (dexamethasone, rituximab, cyclophosphamide) was initiated, renal function declined to end-stage kidney failure, requiring hemodialysis. The M-protein has since disappeared, and hematologic remission has been achieved, but maintenance dialysis continues.
Discussion:
In LPL, renal impairment is typically attributed to hyperviscosity syndrome or massive intraglomerular IgM deposition caused by excessive IgM-type M-protein, as seen in Waldenström’s macroglobulinemia. In this case, however, despite only a mild elevation of serum IgM, the glomeruli exhibited markedly dense deposits. Recently, intracapillary monoclonal IgM glomerulopathy (ICMG-IgM) - formerly termed intracapillary monoclonal deposits disease (ICMDD) - has been proposed as a renal lesion associated with IgM-type monoclonal gammopathy secondary to LPL, and this case consistent with that concept. Notably, the deposits in this case displayed an organized microtubular structure, a feature usually absent in typical ICMG-IgM, making this a particularly intriguing and valuable case.
