ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO0667

Remission Trajectories of Targeted-Release Budesonide Across Mesangial Hypercellularity, Endocapillary Hypercellularity, Segmental Sclerosis, Tubular Atrophy, and Crescent Formation (MEST-C) Phenotypes in IgAN

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • He, Dafeng, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Xu, Jun, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Bo, Gao, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Jiang, Mingzhu, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Liu, Wenjin, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Zhao, Chuanyan, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Li, Xinrui, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Lu, Chunlei, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Zhu, Mengyue, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Mou, Hongbin, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
  • Bi, Guangyu, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China
Background

Targeted-release (TR) budesonide provides upstream mucosal immunomodulation in IgA nephropathy (IgAN),with clinical trial evidence supporting its efficacy in proteinuria reduction and renal function preservation. While trials confirm its efficacy, the impact of downstream structural chronicity on real-world remission trajectories remains insufficiently characterized. Furthermore, the translational relevance of specific active inflammatory phenotypes requires validation.

Methods

We retrospectively analyzed 57 adults with primary IgAN treated with TR-budesonide for ≥6 months. Median percent proteinuria change was assessed at 3, 6, and 12 months. Multivariable models evaluated predictors of 3-month early response and 12-month composite remission (complete/partial), focusing on concomitant SGLT2 inhibitor (SGLT2i) use and endocapillary hypercellularity (E1). These predictors informed a time-dependent prognostic nomogram, validated via optimism-corrected bootstrapping.

Results

The cohort (mean age 40.9±8.3 years) had a baseline eGFR of 61.3±25.2 mL/min/1.73m2 and median proteinuria of 1.21 g/day (IQR 0.60–2.38). MEST-C S1 and T1/T2 lesions were present in 91.2% and 63.2% of biopsies, respectively. At 12 months, median proteinuria declined to 0.40 g/day (57.1% relative reduction), with comparable reductions across all MEST-C strata. Concomitant SGLT2i therapy independently predicted 3-month response (OR 9.40, P=0.023). E1 emerged as the sole independent predictor of 12-month composite remission (OR 2.20, P=0.022), correlating with shorter time to remission (log-rank P=0.031). A derived 10-variable nomogram predicted 12-month remission with an AUC of 0.84.

Conclusion

The antiproteinuric efficacy of TR-budesonide is maintained across MEST-C phenotypes, including advanced structural chronicity. Concomitant SGLT2i drives an early clinical response, while E1 identifies a distinct inflammatory phenotype predictive of long-term remission. Our internally validated nomogram translates these variables into a practical tool for personalized treatment stratification.

Acknowledgment

The authors acknowledge the Ethics Committee of Northern Jiangsu People's Hospital for reviewing and approving this study.

Figure1. Efficacy and remission kinetics of TR-budesonide.