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Basement membrane charge in human glomerular disease.

P N Furness, D R Turner, R E Cotton

    The Journal of Pathology
    |December 1, 1986
    PubMed
    Summary
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    Fixed anionic charges in the glomerular basement membrane are crucial for kidney filtration. This study found that in most human kidney diseases, these charges persist, suggesting proteinuria isn't typically caused by charge loss.

    Area of Science:

    • Nephrology
    • Renal Pathology
    • Cell Biology

    Background:

    • Anionic charges in the glomerulus are key to the filtration barrier.
    • Loss of these charges is linked to proteinuria.
    • Previous studies were limited to experimental models due to tissue fixation requirements.

    Purpose of the Study:

    • To investigate glomerular basement membrane charge in human kidney disease using archival tissue.
    • To determine if proteinuria in humans is associated with a loss of anionic charge.

    Main Methods:

    • Utilized the polyethyleneimine technique on human kidney tissue reprocessed from paraffin blocks (up to 10 years old).
    • Examined cases with confirmed glomerular disease diagnoses.
    • Visualized ultrastructural anionic charges on glomerular basement membranes.

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    Main Results:

    • A continuous anionic charge layer persisted in the majority of human glomerular diseases, even with severe basement membrane abnormalities.
    • Exceptions included amyloidosis (decreased/lost charge) and Systemic Lupus Erythematosus (defects in charge layer).
    • Findings contrast with animal models where charge loss is reported.

    Conclusions:

    • Proteinuria in most human glomerular diseases is likely not caused by extensive loss of glomerular basement membrane anionic charge.
    • The persistence of charge in human disease suggests different pathomechanisms compared to animal models.
    • This study provides insights into the glomerular filtration barrier in human renal pathology.