Abstract: TH-PO0547
How Late Is Too Late? Treating Advanced IgAN
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
- Deshpande, Tanvi, Loma Linda University, Loma Linda, California, United States
- Rana, Janhvi, Loma Linda University, Loma Linda, California, United States
- Norouzi, Sayna, Loma Linda University, Loma Linda, California, United States
Introduction
Targeted-release budesonide (Nefecon) is designed to target Peyer’s patches reducing galactose-deficient IgA1 production and mitigating kidney damage in the setting of IgA nephropathy (IgAN). Nefecon received full FDA approval in December 2023 for patients with IgA nephropathy at risk of progression. The recommended treatment is 9 months followed by 2-week taper. Data in patients with more advanced CKD, especially those with eGFR <30 mL/min remain limited. We present a case where Nefecon was initiated at a GFR below the pivotal trial range with stabilization of kidney function, followed by marked decline after discontinuation and eventual stabilization after re-initiation.
Case Description
A 47-year-old male with biopsy-proven IgAN on lisinopril and dapagliflozin was referred for progressive eGFR decline from 42 to 34 mL/min over a year. Urinalysis showed hematuria and UPCR 0.9. Kidney biopsy showed chronic IgAN with MEST-C M0 E0 S0 T2 C0. As eGFR was below trial thresholds, he was started on Nefecon after discussion of options. eGFR improved to 42-44 mL/min in 3 months and UPCR to 0.238 in 9 months. After 9 months, Nefecon was tapered and discontinued. Three months later, eGFR dropped to 26-30 and UPCR increased to 0.6. Repeat biopsy showed active IgAN with MEST-C M0 E0 S2 T2 C0 and 87% glomerular obsolescence. Nefecon was restarted. Over the next months, eGFR stabilized at 38-42 mL/min and proteinuria improved.
Discussion
In our case, the patient had biopsy-proven IgAN with an eGFR below the range studied in major trials. Kidney function improved after starting Nefecon, but declined after discontinuation despite maximal supportive therapy. Repeat biopsy showed active IgAN with MEST-C score M0 E0 S2 T2 C0, and kidney function stabilized again after Nefecon restarted. This pattern suggests a possible re-treatment-responsive phenotype, or apparent Nefecon dependence, in primary IgAN with advanced CKD. This case adds to the limited evidence on repeat-course Nefecon in advanced CKD and suggests that some patients may benefit from re-initiation.