Abstract: TH-PO0429
Concurrent Collapsing Glomerulopathy and C1q Nephropathy: A Dual Glomerular Injury Pattern Presenting with Persistent Nephrotic Syndrome
Session Information
- Glomerular Diseases: Autoimmune Diseases
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Authors
- Kadavanu, Tony Mathews, Cleveland Clinic Foundation, Weston, Florida, United States
- Cohen, Scott D., Cleveland Clinic Foundation, Weston, Florida, United States
- Pabon-Vazquez, Elizabeth, Cleveland Clinic Foundation, Weston, Florida, United States
- Kuperman, Michael Benjamin, Cleveland Clinic, Cleveland, Ohio, United States
Introduction
Collapsing glomerulopathy (CG) is a severe podocytopathy associated with rapid kidney function decline.C1q nephropathy is a rare immune complex (IC)-mediated glomerular disease characterized by dominant mesangial C1q deposition without SLE.Concurrent CG and C1q nephropathy is uncommon and may represent overlapping pathogenic mechanisms
Case Description
A 45-year-old man presented with nephrotic syndrome with 16.5 g/day proteinuria,eGFR 50-60 mL/min/1.73m2 ,hypoalbuminemia (1.9g/dL) and hypercholesterolemia (550mg/dL).Serologic evaluation showed low-titer ANA positivity (1:40),while autoimmune and infectious studies were otherwise negative.Kidney biopsy demonstrated dual pathology with collapsing glomerulopathy and mesangioproliferative glomerulonephritis with 7/30 glomeruli showing segmental capillary collapse with visceral epithelial hyperplasia.Mesangial hypercellularity, 30% interstitial fibrosis and tubular atrophy were present.IF revealed mesangial IgG, IgM, C3, and dominant C1q (2+) staining.Although kappa staining exceeded lambda,there was no definite light-chain restriction.IgG subclass analysis showed IgG1 and IgG3 predominance without IgG2 or IgG4, supporting a polyclonal process and arguing against proliferative glomerulonephritis with monoclonal IgG deposits.EM confirmed mesangial electron-dense deposits and diffuse podocyte effacement.Viral and medication-related causes of CG were excluded.Initial corticosteroid therapy was limited by low dosing and poor adherence.Genetic testing identified APOL1 high-risk genotype.Cyclosporine therapy is planned.
Discussion
This case highlights a rare overlap between IC-mediated glomerular injury and severe podocytopathy.The coexistence of proliferative C1q nephropathy with CG suggests IC injury may trigger podocyte collapse in genetically susceptible individuals like those with APOL1 risk variants.Recognition of this overlap supports evaluation for genetic susceptibility risk factors which may alter therapy.
Acknowledgment
AI-assisted tools were used to improve the fluency and academic tone of the abstract. All revisions were carefully reviewed and approved by the authors, who take full responsibility for the accuracy and integrity of the final content
a - EM - mesangial deposits
b - Collapsing GN