Abstract: SA-PO0705
Atypical Presentation of C3 Glomerulopathy in a 28-Year-Old Man
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
- Baloch, Kanwal Mir, The University of New Mexico, Albuquerque, New Mexico, United States
- de Leoz, Josephine B., The University of New Mexico, Albuquerque, New Mexico, United States
Introduction
C3 glomerulopathy (C3G) is a complement-mediated kidney disease with dominant glomerular C3 deposition. We report an atypical case of suspected C3G with histologic resolution after conservative therapy in a patient with erythrocytosis and persistent lupus anticoagulant positivity
Case Description
28-year-old male with hypertension, erythrocytosis, and proteinuria (peak urine protein-creatinine ratio 1.9 g/g) underwent kidney biopsy showing mesangial-capillary glomerulopathy with dominant C3 deposition and positive C5b-9 staining, consistent with C3 glomerulopathy (C3G). Evaluation for paraproteinemia, infection, and genetic causes was unrevealing. Complement studies were normal except elevated soluble C5b-9 and properdin. Persistent erythrocytosis and lupus anticoagulant positivity were present.
He was treated with lisinopril and empagliflozin. Repeat biopsy at 6 months showed resolution of C3 deposits and improved mesangial hypercellularity, though moderate interstitial fibrosis and tubular atrophy persisted. Proteinuria improved to 0.16 g/g with stable kidney function (creatinine 1.2 mg/dL). No complement therapy was used.
Discussion
This case demonstrates an atypical course of suspected C3G with complete histologic resolution after conservative therapy alone. Despite complement activation, no complement dysregulation or genetic abnormality was identified, suggesting a transient or secondary process.
Persistent erythrocytosis and lupus anticoagulant positivity raise concern for an antiphospholipid-related mechanism, as complement activation contributes to antiphospholipid-associated microvascular injury. Although the patient remains in clinical and histologic remission, recurrence remains possible given the unclear pathogenesis. This case suggests select patients may be managed conservatively and that repeat biopsy may provide important diagnostic and prognostic value.