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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.
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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.
Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare glomerulonephritis, accounting for only 0.2% of native kidney biopsies. It results from monoclonal immunoglobulin deposition due to clonal plasma or B-cell proliferation, leading to glomerular injury. The clinical manifestations of PGNMID encompass proteinuria, hematuria, and renal impairment, which typically progress chronically in the absence of appropriate treatment. However, acute deterioration of kidney function necessitating dialysis is infrequent during the course of PGNMID. We report a case of PGNMID with severe AKI requiring hemodialysis following recovery from infectious enteritis, successfully managed by clone-directed therapy, including daratumumab and bortezomib.
A 60-year-old man presented with proteinuria and edema. Laboratory tests showed creatinine 1.2 mg/dL, albumin 3.0 g/dL, and urinary protein 5.3 g/gCr. Serum and urine immunofixation were negative, and the free light-chain ratio showed no restriction. Renal biopsy revealed mesangial and endocapillary proliferation with granular IgG3-λ deposits, consistent with PGNMID. He was treated with steroid pulse therapy followed by oral prednisolone and an ARB, later combined with cyclosporine and an SGLT2 inhibitor, achieving partial remission. Two years later, he developed infectious enteritis with pre-renal AKI, which resolved after fluid therapy. Two weeks later, he relapsed with edema, ascites, a 6 kg weight gain, nephrotic-range proteinuria (5.5 g/gCr) and AKI (creatinine 3.4 mg/dL). Repeat biopsy showed marked mesangial and endocapillary proliferation with IgG3-λ deposits.
Steroid therapy was ineffective, and temporary hemodialysis was required. Clone-directed therapy with daratumumab resulted in renal recovery, allowing discontinuation of dialysis. Serum creatinine stabilized at 2.5 mg/dL, with improved proteinuria and hematuria. The patient continues daratumumab therapy as an outpatient.
Cases of PGNMID have been documented following infection with enteritis, Parvovirus B19 or COVID-19, as well as subsequent to COVID-19 vaccination. These observations imply that transient immune irregularities induced by antigenic stimulation may facilitate the proliferation of B-cell and plasma cell clones, thereby augmenting the production of monoclonal IgG and contributing to the initiation or recurrence of PGNMID. The efficacy of clone-directed therapy for PGNMID has been increasingly reported in recent years. Prospective studies are essential to establish optimal treatment strategies for PGNMID with AKI. The current case indicates that the narrowing of the glomerular capillary lumina, resulting from an increase in inflammatory cells and mesangial matrix expansion, may lead to AKI.
