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Related Experiment Videos

Sequential study of the IgA system in relapsing IgA nephropathy.

J Feehally, T J Beattie, P E Brenchley

    Kidney International
    |December 1, 1986
    PubMed
    Summary

    In IgA nephropathy (IgAN) relapse, particularly during upper respiratory tract infections (URTI), immune responses show significant changes. These indicate an exaggerated IgA immune response may trigger kidney damage and hematuria in IgAN patients.

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    Clinical nephrology·2011

    Area of Science:

    • Immunology
    • Nephrology
    • Gastroenterology

    Background:

    • IgA nephropathy (IgAN) is a common glomerular kidney disease.
    • The role of the IgA immune system in IgAN pathogenesis is under investigation.
    • Mucosal immunity and IgA production are key areas of focus.

    Purpose of the Study:

    • To investigate cellular and immunochemical parameters of the IgA system in IgAN patients during relapse and remission.
    • To compare IgA system responses in IgAN patients with those in healthy controls during upper respiratory tract infections (URTI).
    • To explore the link between exaggerated IgA responses and glomerular damage in IgAN.

    Main Methods:

    • Studied 15 IgAN patients and 15 age-matched controls.
    • Assessed IgA-bearing B-lymphocytes, T helper/suppressor cell ratio, and pokeweed mitogen-induced IgA production.

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  • Analyzed total serum and salivary IgA levels.
  • Utilized High-Performance Liquid Chromatography-Enzyme-Linked Immunosorbent Assay (HPLC-ELISA) for serum IgA profiling.

    • Main Results:

    • No IgA system abnormalities were detected in IgAN remission.
    • During IgAN relapse with macroscopic hematuria and URTI, significant increases were observed in IgA-bearing B-lymphocytes, T helper/suppressor cell ratio, and IgA production.
    • Serum IgA profile showed increased polymer IgA during relapse.
    • These changes were not observed in controls during URTI.

    Conclusions:

    • Exaggerated IgA immune responses to mucosal antigen challenge are implicated in initiating glomerular damage and hematuria in IgAN.
    • Specific immune cell populations and IgA production levels are altered during IgAN relapse.
    • Further research into IgA-mediated mucosal immunity is warranted for understanding and treating IgAN.