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.
Immune complex–mediated membranoproliferative glomerulonephritis (IC-MPGN) lacks proven targeted therapy, and many patients remain refractory to corticosteroids and calcineurin inhibitors. Dysregulated alternative-pathway complement activation provides a mechanistic rationale for proximal C3 inhibition. We report a steroid- and tacrolimus-refractory case achieving biochemical and clinical remission with pegcetacoplan.
A 19-year-old man with biopsy-proven IC-MPGN and nephrotic syndrome (24-hour protein 7,988 mg/day; urine protein-to-creatinine ratio [UPCR] 2,502 mg/g; hypoalbuminaemia 20 g/L; microscopic haematuria; C3 0.06–0.14 g/L with normal C4) initiated pegcetacoplan 1,080 mg subcutaneously twice weekly following immunisation against encapsulated organisms. Outcomes included serial proteinuria (24-hour protein; UPCR), serum albumin, complement (C3), kidney function (serum creatinine), blood pressure and safety. Background therapy was tapered according to clinical response.
Pegcetacoplan induced a rapid, sustained antiproteinuric response: 24-hour protein declined to 1,386 mg/day (−83%) and UPCR to 751 mg/g over eight months. Serum albumin normalised (36–38 g/L), C3 rose to 1.27 g/L, and creatinine remained stable (≈89–100 µmol/L). Blood pressure improved, permitting withdrawal of antihypertensives, and tacrolimus was discontinued without recurrence of oedema or haematuria. No adverse events or infectious complications were observed. Baseline histopathology showed an IC-MPGN pattern with granular IgA/IgG/C3 along capillary loops and subendothelial, intramembranous and subepithelial electron-dense deposits; immunoperoxidase demonstrated dominant IgA/IgG with C3, consistent with immune-complex disease.
In IC-MPGN refractory to non-specific immunosuppression, proximal C3 inhibition with pegcetacoplan achieved clinically meaningful remission, normalised complement activity and enabled steroid/calcineurin-sparing. These findings support mechanistic targeting of the alternative pathway in complement-dysregulated disease and justify prospective evaluation to define durability, optimal dosing and biomarkers of response.
