Abstract: SA-PO0707
Real-World Response to Pegcetacoplan in C3 Glomerulopathy: A Two-Case Report
Session Information
- Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Gupta, Sanjeev, Westchester Medical Center, Valhalla, New York, United States
- Mittal, Amol, Westchester Medical Center, Valhalla, New York, United States
- Kapoor, Aromma, Westchester Medical Center, Valhalla, New York, United States
- Chugh, Savneek S., Westchester Medical Center, Valhalla, New York, United States
Introduction
C3 glomerulopathy (C3G) is a rare glomerular disease caused by dysregulation of the alternative complement pathway, leading to excessive C3 protein deposits in the kidney’s glomeruli. It is a rare disease and difficult to treat as no single therapeutic regimen is effective against this disease universally. Pegcetacoplan is a C3/C3b inhibitor and has been found effective in reducing proteinuria in a recent clinical trial. We present 2 cases of biopsy-proven C3G with clinical improvement following pegcetacoplan therapy.
Case Description
A 34-year-old man with substance use disorder was referred for evaluation of elevated serum creatinine (Cr) of 1.7 mg/dL. Urinalysis showed 2+ protein and 21 red blood cells per high-power field, and urine protein-creatinine ratio (UPCR) was 1.0 g/g. Kidney biopsy demonstrated C3G. Despite treatment with prednisone and mycophenolate mofetil (MMF), Cr worsened to 2.4 mg/dL, and UPCR increased to 2.0 g/g. Pegcetacoplan was subsequently initiated, after which Cr improved to 1.0 mg/dL, and UPCR decreased to 0.2 g/g.
A 35-year-old woman with asthma was referred for proteinuria and an elevated Cr of 1.3 mg/dL. Urinalysis showed 3+ protein, and UPCR was 2.5 g/g. Kidney biopsy demonstrated C3G. She was treated with MMF and prednisone, with a reduction in proteinuria to approximately 1.5 g/g. Two years later, Cr increased to 1.8 mg/dL, and UPCR worsened to 2.0 g/g. Pegcetacoplan was then initiated. Afterwards, Cr remained stable at 1.8 mg/dL, and UPCR improved to 1.1 g/g.
Discussion
In patients with C3G, despite treatment, the risk of progression to end-stage kidney disease remains high, reaching 30% to 50% in 10 years. In kidney transplant recipients, the recurrence rate is about 50%. These 2 cases suggest potential benefit of pegcetacoplan in biopsy-proven C3G, especially in patients with persistent proteinuria or worsening kidney function despite conventional immunosuppressive therapy. Given the limited real-world experience with pegcetacoplan in C3GN, these cases add to the emerging evidence supporting complement-targeted therapy in this difficult-to-treat disease.