Abstract: FR-PO0945
Secondary FSGS and Control of Proteinuria with Cyclosporine: A Case Report
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Kharabaf, Sohrab, University of California Irvine School of Medicine, Irvine, California, United States
- Nguyen, Matthew Duy Thanh Luyen, University of California Irvine School of Medicine, Irvine, California, United States
- Le, Dao, UCI Medical Center, Orange, California, United States
- Hanna, Ramy Magdy, UCI Medical Center, Orange, California, United States
Introduction
Focal segmental glomerulosclerosis (FSGS) is a glomerular injury pattern characterized by segmental scarring and proteinuria, often progressing to chronic kidney disease (CKD) or end-stage renal disease (ESRD). It can be primary (idiopathic) or secondary to factors such as obesity, hypertension, or reduced nephron mass. Differentiating between these forms is essential for management. While corticosteroids are used for primary FSGS, secondary FSGS is typically treated by addressing underlying causes. Calcineurin inhibitors (CNIs), such as cyclosporine, have shown efficacy in steroid-resistant primary FSGS, but their role in secondary FSGS remains unclear due to concerns about nephrotoxicity.
Case Description
A 21-year-old male with biopsy-confirmed FSGS diagnosed at age 11 presented with persistent proteinuria despite ACE inhibitor therapy and blood pressure control. His creatinine remained stable (0.7–0.9 mg/dL), but UPCR was consistently 1.0–2.0 g/g. Prednisone was initiated in 2019 and gradually tapered. In 2023, genetic testing revealed variants of uncertain significance (VUS) in INF2 and FN1, genes linked to glomerular disease. Due to persistent proteinuria, cyclosporine was started at 25 mg twice daily and increased to 50 mg twice daily. Over several months, UPCR declined to 0.5 g/g. Renal function remained stable, and blood pressure was controlled at 110–125 mmHg systolic. The patient remained asymptomatic and adhered to dietary sodium restriction, weight management, and continued enalapril. Cyclosporine trough levels and renal function were regularly monitored, with no signs of nephrotoxicity.
Discussion
This case illustrates the potential benefit of cyclosporine in secondary FSGS when conservative therapy is insufficient. Although CNIs are generally reserved for primary or steroid-resistant cases, their use may be justified in select secondary FSGS patients, particularly with suspected genetic predisposition. INF2 and FN1 VUS raise the possibility of an inherited component, though pathogenicity is uncertain. The patient’s response supports the consideration of cyclosporine in secondary FSGS, with careful monitoring. This case highlights the importance of individualized treatment and the need for further studies on CNIs and genetic contributions in secondary FSGS.