Abstract: TH-PO0553
Combination Therapy in IgAN: A Patient Treated with Atrasentan and Targeted-Release Budesonide
Session Information
- Glomerular Diseases: IgAN, IgA Vasculitis, and More
October 22, 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
- Rana, Janhvi, Loma Linda University, Loma Linda, California, United States
- Deshpande, Tanvi, Loma Linda University, Loma Linda, California, United States
- Chen Wongworawat, Yan, Loma Linda University, Loma Linda, California, United States
- Norouzi, Sayna, Loma Linda University, Loma Linda, California, United States
Introduction
Treatment of IgA nephropathy has been evolving for the past few years. Per KDIGO guidelines, a shift towards a multi-layer approach targeting various mechanisms of IgA nephropathy has been suggested. But the real-world experience of these therapies together is limited. We present a patient with IgA nephropathy who was treated with supportive care but developed recurrence of proteinuria and hematuria which was eventually stabilized after combination therapy.
Case Description
A 40-year-old male with biopsy-proven IgA nephropathy done 8 years prior, baseline UPCR 171 mg/g, serum creatinine 0.9 mg/dL and eGFR 98 mL/min presented for routine nephrology follow-up with new-onset hematuria, rising proteinuria (UPCR 411 mg/g) and decreased eGFR to 88 ml/ min over 3 months. The patient was already on max tolerated Lisinopril and Farxiga. Repeat biopsy showed active IgAN and minimal fibrosis <5%. Following the biopsy, the patient was switched to atrasentan and achieved an acceptable response, as UPCR improved to 242 mg/g and eGFR of 96. However, 4 months into therapy, proteinuria increased again to 422 mg/g with recurrent hematuria. Nefecon was then added. Following initiation of dual therapy, the patient showed significant improvement with urinalysis demonstrating resolution of hematuria, UPCR decreasing to 232 mg/g, and eGFR stable at 98 mL/min.
Discussion
This case highlights the potential of combining medications with different mechanisms of action in treating IgA nephropathy. The initial fall in the proteinuria with atrasentan suggested benefit from endothelin pathway blockade but the recurrence of hematuria and increased proteinuria suggested that an underlying immune mediated glomerular injury was active. The improvement of proteinuria to <0.3 g/day (remission levels per KDIGO) and resolution of hematuria after starting nefecon suggests upstream control of inflammation.
This pattern supports the concept that combination therapy may be useful in selected patients when residual disease activity persists and warrants investigation in larger trials.