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Acute nephrotoxicity of cisplatin: molecular mechanisms

Luis Alberto Batista Peres, Ademar Dantas da Cunha

    Jornal Brasileiro De Nefrologia
    |January 10, 2014
    PubMed

    Insights

    Cisplatin nephrotoxicity causes acute kidney injury (AKI) in 20% of patients by damaging renal tubular cells. This review details the molecular mechanisms behind this kidney damage.

    Area of Science:

    • Nephrology
    • Toxicology
    • Molecular Biology

    Background:

    • Nephrotoxic drugs cause approximately 20% of acute kidney injury (AKI) cases.
    • Cisplatin nephrotoxicity is a significant limitation in 20% of patients receiving chemotherapy.
    • Cisplatin induces injury in renal tubular epithelial cells.

    Purpose of the Study:

    • To define the pathophysiology and biochemistry of cisplatin nephrotoxicity.
    • To review the primary molecular mechanisms underlying cisplatin-induced tubular toxicity.

    Main Methods:

    • Literature review of existing studies on cisplatin nephrotoxicity.
    • Analysis of molecular and cellular mechanisms of cisplatin-induced kidney damage.

    Main Results:

    • Cisplatin accumulation in renal tissues is a key factor.
    • Cisplatin interferes with mitochondrial, lysosomal, endoplasmic reticulum, nuclear, and cell membrane functions.
    • This interference leads to inflammation and cell death.

    Conclusions:

    • Cisplatin nephrotoxicity involves complex molecular interactions within renal tubular cells.
    • Understanding these mechanisms is crucial for mitigating cisplatin-induced kidney damage.

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