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Antibiotic-related nephrotoxicity

G J Kaloyanides1

  • 1Department of Medicine State University of New York.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|January 1, 1994
PubMed
Summary

Aminoglycoside and beta-lactam antibiotics exhibit kidney toxicity through cellular uptake and intracellular interactions. Protective strategies involve blocking drug-target binding, offering insights into mitigating nephrotoxicity.

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Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Drug-induced kidney injury is a significant clinical concern.
  • Aminoglycosides and beta-lactams are common therapeutic agents with known nephrotoxic potential.
  • Understanding the molecular mechanisms of drug nephrotoxicity is crucial for developing protective strategies.

Purpose of the Study:

  • To elucidate the mechanisms of nephrotoxicity induced by aminoglycosides and beta-lactams.
  • To explore the role of cellular uptake and intracellular targets in drug-induced kidney damage.
  • To identify potential protective agents against drug nephrotoxicity.

Main Methods:

  • Review of existing literature on aminoglycoside and beta-lactam nephrotoxicity.
  • Analysis of cellular uptake pathways, including adsorptive endocytosis and organic anion transport.
  • Investigation of intracellular targets, such as phospholipids and mitochondrial components.
  • Evaluation of the protective effect of polyaspartic acid against aminoglycoside nephrotoxicity.

Main Results:

  • Aminoglycosides enter proximal tubular cells via adsorptive endocytosis, disrupting anionic phospholipid metabolism.
  • Polyaspartic acid protects against aminoglycoside nephrotoxicity by forming complexes with the drugs.
  • Beta-lactams are selectively toxic due to uptake via organic anion transport, with mechanisms including lipid peroxidation and mitochondrial dysfunction.
  • Amphotericin B causes kidney toxicity by interacting with cell membranes, increasing ion permeability.

Conclusions:

  • Drug-concentrating mechanisms in renal tubular cells are key to aminoglycoside and beta-lactam nephrotoxicity.
  • Interference with intracellular targets, including phospholipids and mitochondrial respiration, drives toxicity.
  • Polymeric agents like polyaspartic acid show promise in preventing drug-induced kidney injury.

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