Abstract: TH-PO0852
Recurrent Refractory Nephrotic Syndrome in an Adult with Positive Soluble Urokinase Plasminogen Activator Receptor (suPAR)
Session Information
- Glomerular Case Reports: Potpourri
November 06, 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
- Delp, Crystal, SUNY Downstate Health Sciences University, New York, New York, United States
- De los Santos Berrido, Eunice J, SUNY Downstate Health Sciences University, New York, New York, United States
- Mengal, Fida, SUNY Downstate Health Sciences University, New York, New York, United States
- Milla, Cristian A., SUNY Downstate Health Sciences University, New York, New York, United States
- Suraj, Fnu, SUNY Downstate Health Sciences University, New York, New York, United States
- Nnaji, Okwudili, SUNY Downstate Health Sciences University, New York, New York, United States
- Wei, David Changli, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Reiser, Jochen, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Seshan, Surya V., Weill Cornell Medicine, New York, New York, United States
- Salifu, Moro O., SUNY Downstate Health Sciences University, New York, New York, United States
- Saggi, Subodh J., SUNY Downstate Health Sciences University, New York, New York, United States
Introduction
Nephrotic syndrome is notable for proteinuria, hypoalbuminemia, edema, and increased thrombotic risk. APOL1 gene variants are strongly linked to FSGS and other kidney diseases in patients of African ancestry. Patients with two risk alleles are at higher risk for ESRD and faster progression to dialysis. suPAR, a circulating protein involved in podocyte injury, is an emerging biomarker linked to FSGS activity and prognosis. We present a case of recurrent nephrotic syndrome with suPAR positivity.
Case Description
A 22-year-old male with APOL1 risk allele and FSGS, diagnosed at age 8, first developed nephrotic syndrome at 3. Biopsy at age 7 showed minimal change disease; by 19, pathology revealed 55% glomerulosclerosis and 20–25% interstitial fibrosis. Despite various immunosuppressants (Cyclophosphamide, Cyclosporine, Rituximab), he faced frequent relapses. IVIG induced remission in 2022, but a relapse in 2023 required plasmapheresis. In September 2024, a flare due to medication non-compliance resolved with resumption. In November 2024, he was hospitalized with >7 g/day proteinuria and edema, biopsy now with focal/global glomerulosclerosis, mesangial thickening, IgM staining, and tacrolimus toxicity. suPAR was elevated—the first positive biomarker in his disease (prior nephrin antibodies were negative). Plasmapheresis again led to improvement.
Discussion
Our case displays the challenge of managing FSGS with relapses despite extensive immunosuppressive therapy. His improvement with plasmapheresis, with positive suPAR suggests an active circulating factor in his disease. This emphasizes the need for personalized treatment plans, and the new role of biomarkers like suPAR, for monitoring to predict flares and guide treatment.