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Abstract: TH-PO0502

Psoriasis-Associated IgAN: Clinicopathological Findings from a Matched Case-Control Study and Preliminary Experience with IL-17 Inhibitor (IL-17i) plus Telitacicept Therapy

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Qi, Chenyang, Shanghai Jiao Tong University Medical School Affiliated Ruijin Hospital, Shanghai, China
  • Pan, Xiaoxia, Shanghai Jiao Tong University Medical School Affiliated Ruijin Hospital, Shanghai, China
  • Xie, Jingyuan, Shanghai Jiao Tong University Medical School Affiliated Ruijin Hospital, Shanghai, China
  • Xu, Jing, Shanghai Jiao Tong University Medical School Affiliated Ruijin Hospital, Shanghai, China
Background

The distinct clinicopathological features of psoriasis-associated IgA nephropathy (IgAN-PSO) compared to primary IgAN (IgAN-PRI) remain insufficiently characterized. Optimal treatment strategies that address both the dermatological and renal components of IgAN-PSO have not been established.

Methods

We conducted a retrospective matched case-control study including 31 biopsy-confirmed IgAN-PSO patients and 62 matched primary IgAN controls (Figure1). Clinicopathological and immunological features were compared between 2 groups. For treatment analysis, five IgAN-PSO patients receiving combined IL-17i and telitacicept were each matched (Figure2).

Results

IgAN-PSO patients exhibited significantly higher segmental glomerulosclerosis proportion (0.24±0.18 vs. 0.14±0.13), more frequent interstitial plasma cell infiltration (87.1% vs. 66.1%,) and more severe renal tubular lesions compared to IgAN-PRI (P all <0.05) . Serum IgG, IgA and C4 were significantly elevated in IgAN-PSO (P all <0.05). Among the five IgAN-PSO patients treated with IL-17i and telitacicept (baseline CLIN-PATH 5-year ESRD risks: 17.57%, 14.11%, 0.49%, 0.77%, 2.18%), all achieved marked proteinuria reduction (3975→515 mg/24h over 20 months; 326.5→100 mg/24h over 3 months) with stable or improved eGFR, outperforming matched comparators on conventional therapy.

Conclusion

IgAN-PSO is pathologically distinct from primary IgAN, with greater glomerulosclerosis, plasma cell infiltration, tubular injury, and immunoglobulin dysregulation reflecting psoriasis-driven B-cell activation. Preliminary evidence supports combined IL-17 inhibitor and telitacicept therapy as a rational approach for IgAN-PSO. Prospective controlled trials are warranted.

Acknowledgment

We are grateful to Professor Anthony Chang from University of Chicago for his valuable insights and constructive suggestions that improved this work. We sincerely thank Dr. Pingyan Shen for her guidance and support, as well as her rich clinical expertise.

Funding

  • Government Support – Non-U.S.