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Related Experiment Videos

[Aminoglycoside nephropathy].

U Burchardt, G Schinköthe, K Meinel

    Zeitschrift Fur Die Gesamte Innere Medizin Und Ihre Grenzgebiete
    |June 15, 1982
    PubMed
    Summary
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    Aminoglycoside antibiotics cause kidney tubule cell damage, increasing lysosomes and impairing kidney function. These effects are reversible, but co-administration with other drugs exacerbates toxicity.

    Area of Science:

    • Nephrology
    • Cell Biology
    • Pharmacology

    Context:

    • Aminoglycoside antibiotics are widely used but can cause nephrotoxicity.
    • Kidney tubule cells are a primary target for aminoglycoside-induced damage.
    • Lysosomes play a critical role in cellular response to aminoglycosides.

    Purpose:

    • To elucidate the cellular mechanisms underlying aminoglycoside-induced nephropathy.
    • To investigate the role of lysosomes in aminoglycoside accumulation and toxicity.
    • To present a hypothesis on aminoglycoside nephrotoxicity.

    Summary:

    • Aminoglycosides increase the number and size of secondary lysosomes in renal tubule cells, leading to myeloid body formation.
    • Accumulation of aminoglycosides in the kidney results in altered tubule cell function, including hyperenzymuria, reduced protein reabsorption, and decreased urine concentration.

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  • Observed functional deviations are reversible upon continued drug exposure, though co-administration with cephalotin, dextran, or furosemide potentiates toxicity.

    • Impact:

    • This research identifies lysosomes as the primary site of action for aminoglycosides in the kidney.
    • Understanding these mechanisms can inform strategies to mitigate aminoglycoside nephrotoxicity.
    • The findings contribute to a comprehensive hypothesis of aminoglycoside-induced kidney damage, considering cellular uptake and lysosomal accumulation.