Abstract: SA-PO0718
The Complement Paradox: C3 Glomerulonephritis with Normal C3 and Recovery Without Immunosuppressive Therapy
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
- Tamang Waiba, Anita, Centinela Hospital Medical Center, Inglewood, California, United States
- Waiba Tamang, Suman, Kantipur Dental College Teaching Hospital & Research Center, Kathmandu, Central Development Region, Nepal
- Wallace, ViolaFlorence O.i, Centinela Hospital Medical Center, Inglewood, California, United States
- Shrestha, Harisharan, Centinela Hospital Medical Center, Inglewood, California, United States
- Rojas Torres, Diana S., Centinela Hospital Medical Center, Inglewood, California, United States
- Pak, Firooz, Centinela Hospital Medical Center, Inglewood, California, United States
Introduction
C3 glomerulonephritis (C3GN) is a rare complement-mediated renal disease usually marked by low serum C3 level. Renal biopsy remains essential for diagnosis. Immunosuppression is considered when proteinuria is ≥1.5 g/day or kidney function worsens, while milder cases can be managed conservatively. This case shows the diagnostic and management challenges of C3GN.
Case Description
A 58-year-old man with history of hypertension and diabetes mellitus presented with acute kidney injury (serum creatinine 3.5 mg/dL), microscopic hematuria (25-50 RBC/hpf) and nephrotic-range proteinuria (UPCR 4 g/g). Renal ultrasound showed small echogenic kidneys, suggesting chronic intrinsic disease. Immunological workup was notable for a normal serum C3 (86 mg/dL) and low C4 level. SPEP ruled out monoclonal gammopathy. Concurrent Enterococcus faecalis bacteremia was identified and treated. A renal biopsy confirmed C3GN with a mesangial proliferation and acute tubular necrosis (ATN).
He was managed conservatively without immunosuppression. Following the treatment of the bacteremia and resolution of the ATN, renal function improved significantly, with serum creatinine improving at 1.2 mg/dL and proteinuria to 1+.
Discussion
This case shows a “Complement Paradox,” where C3GN can occurs despite normal C3. The normal C3 may represent early disease with intrarenal consumption balanced by hepatic synthesis, while low C4 suggests infection-related lectin pathway activation. C3GN remains a differential regardless of systemic markers, mandating tissue diagnosis.
A key takeaway is to identify and treat reversible conditions before initiating long-term immunosuppression. Despite meeting initial criteria for immunosuppression, the patient's rapid recovery through supportive care only avoided the risks of unnecessary therapy.
H&P
Renal recovery