Abstract: SA-PO0770
A Case of Monoclonal Gammopathy of Renal Significance Presenting as C3 Glomerulonephritis
Session Information
- Glomerular Diseases: Lupus Nephritis, Monoclonal Gammopathy-Related Disease, and Transplantation
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
- Deshpande, Tanvi, Loma Linda University, Loma Linda, California, United States
- Wang, Jessie Zheng, Loma Linda University, Loma Linda, California, United States
- Khairullah, Quresh T., VA Loma Linda Healthcare System, Loma Linda, California, United States
Introduction
The usual manifestation of kidney injury in multiple myeloma is through deposition of monoclonal proteins within various kidney structures or cast nephropathy. However, monoclonal proteins can also dysregulate the alternative complement pathway by inhibiting regulatory proteins such as factor H or through other incompletely defined mechanisms. We present a case of monoclonal gammopathy of renal significance (MGRS) resulting in C3 glomerulonephritis (C3GN) with evidence of complement pathway activation.
Case Description
A 78-year-old male presented with progressive loss of kidney function over one year with decline in eGFR from 60 to 15 mL/min. Urinalysis showed RBCs and RBC casts with urine protein-creatinine ratio of 1.9. Serum protein electrophoresis revealed a M spike, elevated free lambda light chains, with a normal kappa/lambda ratio. Bone marrow biopsy demonstrated 4–6% lambda-restricted plasma cells and 10.5% CD5+ monotypic B cells. Kidney biopsy revealed crescentic proliferative glomerulonephritis with immunofluorescence showing high intensity C3 mesangial staining and no immunoglobulin deposits. Complement testing showed borderline low C3 with elevated soluble C5b-9, while factor H activity and C3 nephritic factor were normal. There was absent IgG staining and lack of prior infection, so post infectious GN was deemed unlikely. The overall findings favored MGRS associated C3GN due to monoclonal immunoglobulin mediated alternative complement pathway dysregulation. He was treated with CyBorD (Cyclophosphamide, Bortezomib, and Dexamethasone). C3 levels normalized after treatment. Renal recovery occurred over 6 months with current eGFR 28–30 mL/min.
Discussion
C3GN is a proliferative glomerulonephritis resulting from the dysregulation of the alternative complement pathway. As highlighted in this case, MGRS can present as C3GN via a rare mechanism in which monoclonal immunoglobulins trigger persistent complement activation and glomerular C3 deposition. It is important to recognize that renal pathology findings would reveal high-intensity C3 deposition in the mesangium with the absence of heavy- or light-chain deposits. Early recognition is critical and treatment should target treating the underlying clonal disorder.