The Mechanism of Drug Nephrotoxicity and the Methods for Preventing Kidney Damage

Ewa Kwiatkowska1, Leszek Domański1, Violetta Dziedziejko2

  • 1Clinical Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University, 70-111 Szczecin, Poland.

Insights

Drug-induced acute kidney injury (AKI) affects millions globally. This review details three mechanisms of drug nephrotoxicity: tubular injury, obstruction, and interstitial nephritis, along with risk factors and prevention strategies.

Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Acute kidney injury (AKI) is a significant global health issue, affecting approximately 13.3% of the world's population annually.
  • Key causes of AKI include sepsis, ischemia, and nephrotoxicity, with drug-induced nephrotoxicity accounting for 19-26% of hospitalized cases.

Purpose of the Study:

  • To elucidate the distinct mechanisms of drug-induced nephrotoxicity.
  • To correlate specific drug classes with particular types of kidney injury.
  • To discuss risk factors and preventive or therapeutic strategies for drug-induced AKI.

Main Methods:

  • Review of existing literature on drug-induced nephrotoxicity.
  • Categorization of nephrotoxic mechanisms into tubular injury, tubular obstruction, and interstitial nephritis.
  • Analysis of dose-dependent and dose-independent pathways.

Main Results:

  • Drug-induced nephrotoxicity occurs via three primary mechanisms: proximal tubular injury/acute tubular necrosis (ATN), tubular obstruction by drug crystals/casts, and interstitial nephritis.
  • Proximal tubular injury and tubular obstruction are typically dose-dependent, while interstitial nephritis is dose-independent.
  • Specific drug groups are associated with each of these injury types.

Conclusions:

  • Understanding the mechanisms of drug-induced AKI is crucial for effective management.
  • Identification of risk factors and implementation of preventive measures can mitigate the incidence of drug nephrotoxicity.
  • Further research into targeted therapies for drug-induced kidney injury is warranted.

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