Kidney Week

Abstract: TH-PO818

Understanding the Nature of IgA Deposits in Secondary Glomerular Diseases

Session Information

• Glomerular Diseases: Immunology and Inflammation - I
  October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1202 Glomerular Diseases: Immunology and Inflammation

Authors

• Satoskar, Anjali A., Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Anjali A. Satoskar,

• Malvar, Ana, HOSPITAL FERNANDEZ, Buenos Aires, Argentina

Ana Malvar,

• Alberton, Valeria Gabriela, HOSPITAL FERNANDEZ, Buenos Aires, Argentina

Valeria Gabriela Alberton,

• Bott, Cherri N., Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Cherri N. Bott,

• Nadasdy, Tibor, Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Tibor Nadasdy,

• Nadasdy, Gyongyi, Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Gyongyi Nadasdy,

• Rovin, Brad H., Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Brad H. Rovin,

Background

Galactose-deficient IgA1 (Gd-IgA1) is important to the pathogenesis of primary IgA nephropathy (IgAN) and Gd-IgA1 is found in the glomeruli of IgAN. Other glomerular diseases mimic IgAN and feature significant glomerular IgA deposits, but it is not clear if the IgA in these kidneys is galactose-deficient. This study was done to qualitatively assess IgA in the glomerular deposits of patients with Staphylococcal infection-associated IgAN (IA-IgAN) and cirrhosis-associated IgAN (CA-IgAN).

Methods

Double immunofluorescence staining was done on paraffin-embedded kidney biopsies with anti-human IgA and with the monoclonal antibody KM55, which specifically recognizes Gd-IgA1. Kidney biopsies were from United State (US) and Argentine cohorts, and included patients with primary IgAN (n=9) as positive controls, lupus nephritis (LN, n=11) as negative controls, IA-IgAN (n=6) and CA-IgAN (n=5). The Argentine cohort also included 5 additional patients who had proliferative LN with dominant IgA deposits before and after treatment. IgA and Gd-IgA1 were graded semi-quantitatively based on an intensity scale of 0-3.

Results

Gd-IgA1 staining was robust in patients with primary IgAN as expected, and minimal in patients with LN (Table). In patients with CA-IgAN and IA-IgAN staining for Gd-IgA1 was positive but at about half the intensity of primary IgAN (Table). LN patients who had significant glomerular IgA deposits pre- and post-treatment did have detectable Gd-IgA1 at an intensity about half of Argentine primary IgAN. Gd-IgA1 intensity in primary IgAN was less in Argentine patients than US patients.

Conclusion

Galactose-deficient IgA is present in secondary glomerular diseases with IgA-dominant immune complexes. It is not clear if galactose-deficiency is acquired or if the systemic process unmasks intrinsic defects in IgA.

Funding

• Clinical Revenue Support