Abstract: TH-PO0464
Serum Galactose-Deficient IgA1 Levels in IgAN and Other Glomerular Diseases
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
- Zhang, Xiaolan, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
- Ayoub, Isabelle, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
- Rizk, Dana V., Reliant Glycosciences LLC, Birmingham, Alabama, United States
- Julian, Bruce, Reliant Glycosciences LLC, Birmingham, Alabama, United States
- Novak, Jan, Reliant Glycosciences LLC, Birmingham, Alabama, United States
- Placzek, William J., Reliant Glycosciences LLC, Birmingham, Alabama, United States
- Renfrow, Matthew, Reliant Glycosciences LLC, Birmingham, Alabama, United States
- Rovin, Brad, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
Background
Galactose-deficient IgA1 (Gd-IgA1) is considered critical to the development of IgA nephropathy (IgAN) and may be a biomarker of the disease. Characterizing its role in IgAN has been hampered by the lack of an available bioassay to measure Gd-IgA1. Reliant Glycosciences, LLC developed an easy-to-use lectin-ELISA for Gd-IgA1 in serum that we tested in biopsy-proven IgAN patients and compared results to those of individuals with other glomerular diseases.
Methods
Serum was collected from 70 IgAN, 23 lupus nephritis (LN), 20 diabetic kidney disease (DKD) patients (at time of diagnostic biopsy), and from 13 healthy controls (HC). Gd-IgA1 was assessed using the GalDTM Assay kit RG00180 (Reliant Glycosciences LLC, Birmingham, Alabama, USA). ANOVA and multiple linear regressions used IBM SPSS for data analysis.
Results
Serum Gd-IgA1 level was significantly elevated in IgAN patients compared to those of disease controls and healthy individuals (p<0.001). In IgAN serum, Gd-IgA1 was 94±39 μg/ml versus 55±25 μg/ml in LN, 42±28 μg/ml in DKD, and 49±27 μg/ml in HC. Gd-IgA1 in IgAN was 1.7-, 2.0-, and 1.9-fold higher than in LN, DKD, and HC, respectively. Gd-IgA1 level did not correlate with serum creatinine, eGFR, urine protein/creatinine ratio, or complement component 3. Serial serum samples were available from 14 patients followed for an average of 15±17 months. There was no significant difference between the Gd-IgA1 level at biopsy (83±34 μg/ml) and subsequent time points (86±32 μg/ml, p=0.43). There was a trend toward lower Gd-IgA1 in patients who improved over time and higher Gd-IgA1 in patients who worsened over time (Table).
Conclusion
Gd-IgA1 was detected in sera of HC, patients with IgAN and other glomerular diseases, but levels in IgAN were significantly higher. Gd-IgA1 levels were stable within individuals over time, showing some tendency toward increasing or decreasing depending on whether the disease worsened or improved, respectively, although these changes are relatively small. Further studies in larger cohorts are needed to assess its validity as a biomarker to follow disease activity.
Funding
- NIDDK Support – Reliant Glycosciences LLC