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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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Renal involvement in B-cell lymphomas can occur via tumor infiltration or monoclonal immunoglobulin deposition related to monoclonal gammopathy of renal significance (MGRS). Ibrutinib, a Bruton’s tyrosine kinase inhibitor widely used for mantle cell lymphoma (MCL), is associated with hypertension, bleeding, and rarely, renal dysfunction. Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare form of MGRS, usually of the IgG type; IgM-type PGNMID is exceedingly uncommon. We report a rare case of IgM-type PGNMID developing during ibrutinib therapy for MCL.
A 75-year-old man was diagnosed with MCL after endoscopic detection of a gastric ulcerative lesion and He received ibrutinib (560 mg/day). Hypertension developed soon after ibrutinib initiation, requiring antihypertensive therapy. Baseline renal function was normal (serum Cr [sCr] 0.8 mg/dL, no urinary abnormalities). After two years of treatment, gradual deterioration (sCr 1.2 mg/dL) led to dose reduction (280 mg/day). Two months after dose reduction, proteinuria (0.8 g/gCr) and microscopic hematuria (10–19 RBCs/HPF) appeared (sCr 1.36 mg/dL). Serum electrophoresis revealed λ-type monoclonal protein, but bone marrow biopsy showed no evidence of plasma cell proliferation. Four months later, proteinuria increased to 6.7 g/gCr, raising suspicion of ibrutinib-induced nephrotoxicity. After drug withdrawal, proteinuria decreased to 3.5 g/gCr, though renal dysfunction persisted (sCr 1.3 mg/dL). Renal biopsy showed membranoproliferative glomerulonephritis with tubulointerstitial injury. Immunofluorescence demonstrated strong IgM and κ, and was negative for amyloid. Electron microscopy revealed subendothelial and mesangial electron-dense deposits, confirming IgM-type PGNMID with interstitial nephritis. Without immunosuppressive therapy, renal function stabilized (sCr ~1.3 mg/dL), proteinuria improved (<1 g/gCr), and hematuria resolved. Two years later, duodenal lesions indicated MCL relapse. Subsequent VP and CHOP regimens achieved complete remission, and renal function remained stable.
Although ibrutinib-induced nephrotoxicity could not be excluded, renal biopsy confirmed IgM-type PGNMID, suggesting MCL-related monoclonal immunoglobulin deposition as the main cause. IgM-type PGNMID is extremely rare, and its association with MCL has been reported only sporadically. This case highlights the importance of considering MGRS-related glomerulonephritis, in addition to drug-induced injury, when evaluating renal impairment in lymphoma patients.
We describe a rare case of IgM-type PGNMID associated with MCL during ibrutinib therapy. Detailed pathological assessment is essential to distinguish lymphoma-related renal disease from drug-induced injury in patients receiving molecularly targeted agents for B-cell malignancies.
