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Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
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Cisplatin nephrotoxicity

K B Meyer1, N E Madias

  • 1Department of Medicine, New England Medical Center, Boston, MA 02111.

Mineral and Electrolyte Metabolism
|January 1, 1994
PubMed
Summary
This summary is machine-generated.

Cisplatin chemotherapy can harm kidneys, causing acute kidney injury and magnesium loss. While hydration helps prevent acute injury, long-term kidney effects and protective strategies require further investigation.

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Area of Science:

  • Nephrology
  • Oncology
  • Pharmacology

Background:

  • Cisplatin chemotherapy is a vital cancer treatment but frequently causes kidney damage (nephrotoxicity).
  • Clinical manifestations include acute kidney injury and magnesium wasting.
  • Current fluid infusion protocols mitigate acute renal failure but long-term effects remain unclear.

Purpose of the Study:

  • To review the mechanisms of cisplatin-induced kidney injury.
  • To evaluate the effectiveness of various agents in preventing or reducing cisplatin nephrotoxicity.

Main Methods:

  • Review of experimental and clinical studies on cisplatin nephrotoxicity.
  • Analysis of agents that modulate cisplatin uptake, metabolism, and hemodynamic effects.

Main Results:

  • Sulfhydryl metabolism and oxidative stress are key mechanisms in cisplatin kidney injury.
  • Agents like thiosulfates, calcium channel blockers, selenium, and others show potential in altering cisplatin nephrotoxicity.
  • Evidence suggests these agents can modify renal uptake and hemodynamic consequences of cisplatin.

Conclusions:

  • Cisplatin nephrotoxicity is a significant clinical challenge.
  • Understanding the role of sulfhydryl metabolism and oxidative stress is crucial for developing protective strategies.
  • Further research is needed to confirm the long-term efficacy and safety of potential renoprotective agents against cisplatin-induced kidney damage.