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Related Experiment Videos

Glomerulonephritis in ankylosing spondylitis.

K H Shu, J D Lian, Y F Yang

    Clinical Nephrology
    |April 1, 1986
    PubMed
    Summary

    Ankylosing spondylitis (AS) patients frequently show elevated serum IgA levels and kidney issues like IgA nephropathy. This study found a significant association between AS and glomerulonephritis (GN), particularly IgA nephropathy.

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    Area of Science:

    • Nephrology
    • Rheumatology
    • Immunology

    Background:

    • Glomerulonephritis (GN) has been rarely associated with ankylosing spondylitis (AS).
    • Reported GN types include IgA nephropathy, mesangial proliferative GN, and membranous nephropathy.
    • The underlying mechanisms linking AS and GN require further investigation.

    Purpose of the Study:

    • To investigate the prevalence and types of glomerulonephritis in patients with ankylosing spondylitis.
    • To explore the association between serum IgA levels, HLA-B27 antigen, and kidney involvement in AS patients.
    • To discuss the interrelationship between AS and IgA nephropathy.

    Main Methods:

    • Prospective observation of 116 definite AS cases over two years (1983-1984).
    • Clinical and laboratory evaluation of 5 patients diagnosed with GN.

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  • Measurement of serum IgA levels in 78 AS patients and correlation with clinical findings.

    • Main Results:

    • Five cases (4.3%) of GN were identified among 116 AS patients.
    • IgA nephropathy was the most common type (3 cases), followed by mesangial proliferative GN (2 cases).
    • All GN patients exhibited microscopic hematuria; renal function and proteinuria were normal. Elevated serum IgA was observed in most cases, and 63% of AS patients had hypergammaglobulinemia A.

    Conclusions:

    • A significant association exists between ankylosing spondylitis and glomerulonephritis, especially IgA nephropathy.
    • Elevated serum IgA levels are common in AS patients and may indicate kidney involvement.
    • Further research is warranted to elucidate the pathogenesis of GN in AS.