Abstract: SA-PO0627
Rapid Progression in IgAN Despite Treatment: Real-World Evidence of Suboptimal Disease Control in the United States
Session Information
- Glomerular Diseases: Clinical, Outcomes, and Therapeutics Research - Other
October 24, 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
- Paul, Damemarie, Vera Therapeutics Inc, Brisbane, California, United States
- Gao, Emily, Analysis Group Inc, Boston, Massachusetts, United States
- Anderson, Annika, Analysis Group Inc, Boston, Massachusetts, United States
- Goldschmidt, Debbie, Analysis Group Inc, Boston, Massachusetts, United States
- Swallow, Elyse E., Analysis Group Inc, Boston, Massachusetts, United States
- Cockrum, Paul, Vera Therapeutics Inc, Brisbane, California, United States
- Hivale, Phillip, Vera Therapeutics Inc, Brisbane, California, United States
- Keith, Michael, Vera Therapeutics Inc, Brisbane, California, United States
- Tangri, Navdeep, Klinrisk Inc., Winnipeg, Manitoba, Canada
- Jackson, Jay, Vera Therapeutics Inc, Brisbane, California, United States
Background
IgA nephropathy (IgAN) is a B-cell mediated autoimmune disease that causes progressive and irreversible kidney damage. Treatment remains largely reliant on supportive therapies that do not directly target underlying disease mechanisms. Whether these approaches alter disease trajectory in US real-world settings is not well-characterized.
Methods
This retrospective cohort study utilized linked US claims and laboratory data (2020 to 2024) to evaluate disease markers, treatment exposure, and outcomes among adults with ≥1 IgAN diagnosis and renal biopsy. Patients were followed from first diagnosis through available follow-up. Treatment patterns and disease progression endpoints were assessed.
Results
Among the 5,850 patients with IgAN included in the study disease burden was substantial at diagnosis. On average, patients presented at CKD stage ≥3, had proteinuria of 1.3 g/g, and an eGFR of 44.0 mL/min/1.73 m2. Prior to diagnosis, patients were most commonly on renin-angiotensin-aldosterone system inhibitors (RAASi) and corticosteroids.
Treatment was largely unchanged after diagnosis. Among treated patients, RAASi was the dominant therapy (79%). Sodium-glucose cotransporter-2 inhibitors (SGLT2s) were used for 28% of patients with a median time to initiation of 57 days post-diagnosis. Dual Endothelin Angiotensin Receptor Antagonists (DEARAs) and complement inhibitors were used in 2.3% and 0.4% of patients and initiated at a median of 265 and 37 days, respectively. Corticosteroid use was common (61%) and initiated on average 13 days after diagnosis. However, courses were short (median use of 60 days), consistent with episodic use. Budesonide was used in 5.6% of patients.
In this treatment environment, approximately 50% of patients progressed to kidney failure or death within 4.5 years. Among patients with pre- and post-diagnosis eGFR data, 40% had >30% decline by year 4.
Conclusion
Patients with IgAN are commonly diagnosed with advanced disease and are treated with supportive therapies that do not sufficiently slow progression. These data highlight the need for earlier diagnosis. Additionally, the emergence of therapies targeting IgAN upstream pathophysiology represents a critical opportunity to improve long-term renal outcomes.