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A comparative immunologic study of IgA nephropathy.

K Kanatsu, T Doi, K Sekita

    American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
    |May 1, 1983
    PubMed
    Summary
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    This study found that circulating immune complexes (CIC) containing IgA, IgG, or IgM correlate with glomerular deposits in IgA nephropathy patients. A new assay detected IgA CIC, unlike older methods, suggesting mesangial IgA deposits originate from CIC.

    Area of Science:

    • Nephrology
    • Immunology
    • Clinical Chemistry

    Background:

    • IgA nephropathy is a kidney disease characterized by IgA deposits in the glomeruli.
    • The origin and composition of these glomerular deposits are not fully understood.
    • Previous assays for circulating immune complexes (CIC) often failed to detect IgA class CIC.

    Purpose of the Study:

    • To investigate the presence and immunoglobulin class of CIC in patients with IgA nephropathy.
    • To correlate the findings of CIC with glomerular immune deposits.
    • To evaluate the utility of a conglutinin binding assay for detecting IgA CIC.

    Main Methods:

    • Sera from IgA nephropathy patients were tested for CIC using a conglutinin binding assay.
    • The assay detected CIC of IgA, IgG, and IgM classes.

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  • Results were correlated with immunofluorescence and immunoelectronmicroscopic findings of glomerular deposits.
  • Main Results:

    • IgA class CIC were detected in 40.7% of patients.
    • IgG class CIC were found exclusively in patients with glomerular IgG deposits.
    • IgM class CIC were more prevalent in patients with glomerular IgM deposits, showing a correlation between CIC and deposits.

    Conclusions:

    • Conglutinin binding assay effectively detects IgA CIC, which are missed by Clq binding assays.
    • There is a significant association between the immunoglobulin class of CIC and glomerular deposits in IgA nephropathy.
    • Mesangial IgA deposits in IgA nephropathy are likely composed of immune complexes derived from circulating IgA CIC.