Abstract: SA-PO0715
A Case of C3 Glomerulopathy
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
- Kallarackel, Rosemary, Advocate Christ Medical Center, Oak Lawn, Illinois, United States
- Distor, Anndrea, Advocate Christ Medical Center, Oak Lawn, Illinois, United States
- Kedwaii, Hadiah, Advocate Christ Medical Center, Oak Lawn, Illinois, United States
- Fletcher, Nathan R., Advocate Christ Medical Center, Oak Lawn, Illinois, United States
- Kondapi, Goutham, Advocate Christ Medical Center, Oak Lawn, Illinois, United States
Introduction
C3 glomerulopathy (C3G) is a rare immune complex mediated membranoproliferative glomerulonephritis caused by a dysregulation in the alternative pathway resulting in excessive C3, which deposit in the renal glomeruli. This dysregulation can be due to genetic mutations, infection, or secondary to underlying plasma cell dyscrasias.
Case Description
61-year-old African American male with medical history of heart transplant, hypertension, diabetes mellitus, chronic kidney disease 3B, presents with generalized weakness and fatigue. Reports compliance with tacrolimus and myophenelate mofetil (MMF). On admission, creatinine 3.62 mg/dL (from baseline of 2.5 mg/dL), urine analysis (UA) protein of 100 mg/dL, and intial urine protein creatinine ratio (UPCR) 1465 g. The echocardiogram showed an ejection fraction of 70%, IVC with respiraphasic changes. Patient was started on a fluid rate with initial improvement in creatinine but then progressive worsening of kidney function. Was trialed on diuresis with transient improvement in kidney function so further diuresis held. Right heart catheterization showed elevated filling pressures. UPCR worsened to 1.8 g, UA proteinuria increased to 300 mg/dL. Further evaluation included: C3 8 mg/dL, C4 19.5 mg/dL, Kappa 24.88 mg/dL Lambda 17.62 mg/dL. Patient was started on hemodialysis and pulse dose steroids for concern for C3G. Renal biopsy consistent with C3 glomerulonephritis. Bone marrow biopsy negative for multiple myeloma 2% plasma cells consistent with monoclonal gammopathy of undetermined significance. Patient was started on steroids, increased MMF dose, and planned to be started on iptacopan therapy pending insurance approval.
Discussion
C3G is difficult to identify given that its presentation can be similar to other glomerulopathies. This patient presented initially without hematuria, sub-nephrotic range proteinuria, and AKI that progressively worsened despite volume status. Then, upon further investigation and workup, the markedly low C3 raised suspicion for C3G, that prompted diagnosis and initiation of appropriate therapy. This case highlights the importance of early diagnosis and initiation of treatment in hopes to reduce glomerular damage, as a quarter of patients go on to develop end stage kidney disease.