ArticleJournal of translational autoimmunity2026
Proliferative glomerulonephritis with monoclonal IgG3 deposits: A case series.
Article in Journal of translational autoimmunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) caused by IgG3-dominant is rare and incompletely characterized. We retrospectively reported seven male patients (median age 63 years) with IgG3-dominant monoclonal immunoglobulin-associated glomerulonephritis. All patients presented with proteinuria (1.2-16.4 g/24 h), five with nephrotic-range proteinuria, and serum creatinine at diagnosis ranged from 88 to 294 μmol/L. Serum immunofixation electrophoresis was negative in all cases, while urinary free light chains were variably increased. Renal biopsy predominantly demonstrated a membranoproliferative glomerulonephritis pattern (6/7), frequently accompanied by crescents and variable degrees of chronic glomerulosclerosis. Immunofluorescence consistently showed dominant IgG3 deposition. Therapeutic approaches included supportive therapy, corticosteroids combined with cyclophosphamide, ripertamab-based regimens, and bortezomib. Renal outcomes were heterogeneous, ranging from sustained remission to progression to end-stage renal disease or death from severe infectious complications. Patients receiving bortezomib-based clone-directed therapy achieved the most reduction in proteinuria. These findings highlight the marked clinicopathological heterogeneity of IgG3-dominant PGNMID and underscore the importance of early recognition, assessment of chronic histologic injury, and individualized clone-directed treatment to improve renal outcomes.
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