Abstract: TH-PO0485
Significance of Evaluating Glomerular Gd-IgA1 Deposition to Assess Disease Activity
Session Information
- Glomerular Diseases: Clinical, Outcomes, and Therapeutics Research - IgAN
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
- Aoki, Ryousuke, Juntendo Daigaku, Bunkyo, Tokyo, Japan
- Kadota, Nozomi, Juntendo Daigaku, Bunkyo, Tokyo, Japan
- Mori, Kazuaki, Juntendo Daigaku, Bunkyo, Tokyo, Japan
- Nihei, Yoshihito, Juntendo Daigaku, Bunkyo, Tokyo, Japan
- Suzuki, Yusuke, Juntendo Daigaku, Bunkyo, Tokyo, Japan
- Suzuki, Hitoshi, Juntendo Daigaku, Bunkyo, Tokyo, Japan
Background
IgA nephropathy (IgAN) is the most common primary glomerulonephritis and carries a risk of progression to kidney failure. In Japan, tonsillectomy and steroid pulse therapy has been reported to induce clinical remission in approximately 70% of patients. However, histological evaluation after remission remains limited. Galactose-deficient IgA1 (Gd-IgA1) deposited in the glomeruli can be specifically identified with the KM55 monoclonal antibody (KM55 mAb) in IgAN, however glomerular Gd-IgA1 after clinical remission has not been evaluated.
Methods
We performed repeat biopsy on IgAN patients who achieved complete remission (CR) of urinary abnormalities or presented persistent isolated hematuria after immunosuppressive therapy. In present study, patients were included if they achieved CR or had persistent isolated hematuria for ≥four years prior to repeat biopsy. In present study, we included eight patients if they achieved CR (n=6) or had persistent isolated hematuria (n=2). The median interval between biopsies was nine years (range 4–22). In addition to glomerular IgA and C3 immunostaining, Gd-IgA1 deposition were assessed using KM55 mAb. Histological acute and chronic lesions were also evaluated.
Results
In the CR group, glomerular IgA deposition persisted in four of six cases, however, Gd-IgA1 deposition was absent in all cases. In patients with isolated persistent hematuria, both glomerular IgA and Gd-IgA1 deposition were absent, while glomerular thin basement membrane was observed. Histological active lesions, including endocapillary hypercellularity and crescents, were not observed in either group at repeat biopsy.
Conclusion
Glomerular Gd-IgA1 deposition was absent in patients with clinical remission, suggesting that glomerular Gd-IgA1 is a metric of disease activity in IgAN. Persistent isolated hematuria without glomerular Gd-IgA1 deposition may reflect alternative mechanisms, such as structural abnormalities of the thin basement membrane. These findings highlight a complementary role for KM55 staining in disease assessment. Further studies are warranted to validate these findings.