Abstract: SA-PO0734
Late-Onset C3 Glomerulopathy with Atypical Features and Response to Conservative 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
- Rosario González, María del Mar, Department of Medicine, University Hospital Dr. Ramón Ruiz Arnau, Bayamón, Puerto Rico, United States
- Colon Lopez, Stephanie, Private Practice Nephrology, Bayamón, Puerto Rico, United States
- Rodriguez, Eddie M., Department of Medicine, University Hospital Dr. Ramón Ruiz Arnau, Bayamón, Puerto Rico, United States
Introduction
C3 glomerulopathy is a rare complement-mediated kidney disease characterized by dysregulation of the alternative complement pathway and dominant C3 deposition in the glomeruli. It is most often described in children and young adults, and reports in older patients are less common. In clinical practice, distinguishing dense deposit disease from C3 glomerulonephritis can be challenging, particularly in cases with atypical histopathologic findings.
Case Description
A 71-year-old woman with a medical history of well-controlled hypertension, type 2 diabetes mellitus, and nephrolithiasis was referred for evaluation of nephrotic-range proteinuria with a urine albumin to creatinine ratio of 6063 mg/g. She denied hematuria, edema, or other urinary symptoms. Serologic evaluation and genetic testing for secondary causes of proteinuria were unremarkable.
Kidney biopsy demonstrated acute tubular injury on light microscopy. Immunofluorescence showed trace C3 staining without significant immunoglobulin deposition. Electron microscopy revealed scattered subepithelial and mesangial electron-dense deposits. These findings were consistent with a C3 glomerulopathy with features overlapping those seen in dense deposit disease, although classic intramembranous dense deposits were not identified.
The patient was treated with an angiotensin receptor blocker, a sodium glucose cotransporter 2 inhibitor, and a non-steroidal mineralocorticoid receptor antagonist, with marked improvement in proteinuria; therefore, immunosuppressive therapy was not initiated.
Discussion
This case describes an uncommon presentation of C3 glomerulopathy in an older patient with atypical biopsy findings. The absence of characteristic intramembranous dense deposits supports a phenotype more consistent with C3 glomerulonephritis and highlights the overlap within the spectrum of C3 glomerulopathy.
Proteinuria is common in patients with type 2 diabetes mellitus and may lead to missed alternative diagnoses in the absence of kidney biopsy and genetic testing. This case emphasizes the importance of further evaluation in patients with persistent proteinuria or findings atypical for diabetic nephropathy.
The reduction in proteinuria with conservative therapy alone is also notable. Although complement-targeted therapies are increasingly used, selected patients without progressive features may respond to supportive care and individualized management.