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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare kidney manifestation of monoclonal gammopathy characterized by glomerular deposition of a single immunoglobulin subclass and light chain. The IgM subtype (IgM-PGNMID) is particularly uncommon, accounting for approximately 10% of all PGNMID cases, and is often associated with B-cell lymphoproliferative disorders. While evidence regarding IgM-PGNMID is accumulating, the clinical course following diagnosis, especially disease progression, remains unclear. We report a case of IgM-PGNMID associated with lymphoplasmacytic lymphoma (LPL) that progressed to nephrotic syndrome despite sustained serologic remission of the underlying LPL, necessitating repeat kidney biopsy.
A 72-year-old man with a 14-year history of LPL had been treated with corticosteroids and rituximab with a poor response. Hematologic remission was achieved after switching to tirabrutinib three years prior to presentation. However, he developed progressive proteinuria (2.0 g/gCr) with a serum creatinine of 0.9 mg/dL, prompting kidney biopsy.
The biopsy revealed mesangial hypercellularity, double contours of the glomerular basement membrane, and expansion of the subendothelial space. Immunofluorescence showed predominant deposition of IgM and λ light chains. Electron microscopy confirmed non-organized, electron-dense deposits in the mesangial and subendothelial areas, leading to a diagnosis of IgM-PGNMID. Despite ongoing hematologic remission, characterized by low serum IgM levels and no detectable M-protein, the patient's condition rapidly progressed to nephrotic syndrome with declining kidney function, which prompted second kidney biopsy. The repeat biopsy confirmed the progression of interstitial fibrosis and sclerosis without evidence of new-onset glomerulonephritis, reaffirming the diagnosis of IgM-PGNMID. As the LPL was considered well-controlled both serologically and by bone marrow examination, the decision was made to continue tirabrutinib and conservative management, including blood pressure and fluid control. However, three months later, the patient passed away due to a cerebellar hemorrhage.
Serum M-protein is detectable in only approximately 30% of IgM-PGNMID cases. This suggests that a qualitative abnormality of the monoclonal IgM, potentially present at levels below the detection threshold, may predispose it to glomerular deposition. This case demonstrates that kidney disease can progress to nephrotic syndrome due to IgM-PGNMID despite the stable disease activity of the underlying LPL. Furthermore, IgM-PGNMID is associated with a poor kidney prognosis, with a median kidney survival of 44 months. More preserved kidney function at the time of PGNMID diagnosis has been associated with better kidney outcomes, suggesting that early diagnosis is crucial. Even during hematologic remission, kidney disease can persist or progress. This highlights the critical need for close collaboration between hematologists and nephrologists to ensure early diagnosis by kidney biopsy and to determine the optimal treatment strategy.
