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Abstract: FR-PO839

Validation Study of KM55 ELISA Kit in IgA Nephropathy (IgAN) Patients for the Detection of Galactose-Deficient IgA1 (Gd-IgA1) and Corticosteroid Therapy Monitoring

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Kouri, Nikoletta-Maria, Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece
  • Stangou, Maria J., Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece
  • Chiurlia, Samantha, Schena Foundation, Valenzano-Bari, Italy
  • Cox, Sharon N., Schena Foundation, Valenzano-Bari, Italy
  • Ohyama, Yukako, Fujita Health University School of Medicine , Toyoake, AICHI-KEN, Japan
  • Takahashi, Kazuo, Fujita Health University School of Medicine , Toyoake, AICHI-KEN, Japan
  • Papagianni, Aikaterini A., Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece
  • Schena, Francesco Paolo, University of Bari, Bari, Italy
Background

Serum levels of Gd-IgA1 may be considered the first biomarker of IgAN. In the past, Gd-IgA1 was detected by sophisticated methods such as mass spectrometry (MS) and lectin based assay. Recently, a monoclonal antibody KM55 that specifically binds Gd-IgA1 has become commercially available. Aim of our study has been i) to validate this tool, ii) to analyze relationships between serum Gd-IgA1 levels and the outcome of the disease and iii) to study the effect of corticosteroids (CS) on this non-invasive biomarker.

Methods

Serum levels of Gd-IgA1 were measured using ELISA Kit (Immune-Biological Lab. Co. LTD, Japan) in a cohort of 63 IgAN patients, 31 healthy blood donors (BD) and 31 primary non-IgAN (enrolled at the time of kidney biopsy in the Dept of Nephrology, Aristotle Univ of Thessaloniki, Greece). Fourteen IgAN patients were followed-up for a median time of 8.6±6.1 years. High resolution mass spectrometric (HRMS) analysis was used to study 2 IgAN patients with high serum level of Gd-IgA1, 2 IgAN patients with low serum Gd-IgA1 levels and 2 BD, to confirm the profile of IgA1 O-glycoforms.

Results

Patients with IgAN had higher values of Gd-IgA1 (1.53 ± 1.06 mg/dl) than controls (0.90 ± 0.65 mg/dl p=0.002) and patients with non-IgAN (0.89 ± 0.70 mg/dl p=0.001). HRMS analyses confirmed that less O-glycosylated glycoforms were predominantly presented in IgAN patients with high values of Gd-IgA1. A significant reduction of Gd-IgA1 serum levels was found during the follow-up compared to base-line values (n=14 p<0.01). This decline was more prominent in patients who received corticosteroids (n=8, p=0.008). The values of Gd-IgA1 did not influence the progression of renal damage (50% reduction of baseline eGFR).

Conclusion

High Gd-IgA1 serum levels characterize patients with IgAN at the time of kidney biopsy. During the clinical course of the disease Gd-IgA1 levels decline but this reduction is more prominent in patients receiving CS. This biomarker may be used for monitoring the effects of CS therapy