Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Antineutrophil cytoplasmic antibody (ANCA) can cause rapidly progressive glomerulonephritis by inducing crescentic glomerulonephritis. The coexistence of ANCA positivity with a membranoproliferative glomerulonephritis (MPGN) pattern of injury is rare, and the association between ANCA and MPGN is poorly understood. We present a case of myeloperoxidase (MPO)-ANCA-positive MPGN that was successfully treated with immunosuppressive therapy, and discuss the potential contribution of MPO-ANCA to renal injury.
Case presentation; A woman in her 70s referred to our department due to rapidly declining kidney function. She had a history of hypertension and chronic kidney disease and had smoked five cigarettes daily since her 40s. At presentation, laboratory tests revealed severe kidney dysfunction with a serum creatinine of 2.31 mg/dL (compared to her baseline of 1.0 mg/dL three months prior), microscopic hematuria (10-19 erythrocytes per high-power field), and proteinuria (protein-creatinine ratio 3.8 g/g). Serum MPO-ANCA was positive at 72.3 IU/ml. Computed tomography revealed bilateral pleural effusion and interstitial pneumonia. Based on the clinical presentation of rapidly progressive glomerulonephritis (RPGN), interstitial pneumonia, and MPO-ANCA positivity, we initially diagnosed microscopic polyangiitis (MPA). Intravenous methylprednisolone pulse therapy was administered for 3 days starting on day 7, followed by oral prednisolone. Weekly intravenous rituximab was added from day 14. Although hemodialysis was initiated on day 23, kidney function gradually improved, and dialysis was discontinued on day 61. Her serum creatinine level is currently stable approximately 3.0 mg/dL.
Renal biopsy revealed diffuse global glomerular membrane thickening with mesangial and endocapillary hypercellularity; one of the 12 glomeruli showed cellular crescent formation. Immunofluorescence studies demonstrated no significant immunoglobulin or complement deposition, and electron microscopy showed only minimal focal segmental subendothelial and intramembranous deposits. MPO immunostaining revealed scattered MPO-positive cells within the glomeruli, indicating neutrophil infiltration. These findings were consistent with active MPGN that was neither immunoglobulin/immune complex- nor complement-mediated, rather than necrotizing crescentic glomerulonephritis.
MPGN with ANCA positivity is rare, and comprehensive reports are lacking. However, studies of ANCA-positive lupus nephritis have demonstrated higher frequencies of active lesions, including endocapillary hypercellularity and crescent formation, suggesting that ANCA may increase disease activity in underlying glomerulonephritis. In ANCA-associated vasculitis, MPO-ANCA activates neutrophils as a key pathogenic mechanism. In our case, pathological findings revealed MPGN with active lesion, and MPO immunostaining demonstrated scattered MPO-positive cells within the glomeruli. These findings suggest that ANCA-mediated neutrophil inflammation may have enhanced disease activity in underlying MPGN, which showed the favorable response to immunosuppressive therapy.
