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Molecular pathways driving omeprazole nephrotoxicity.

Miguel Fontecha-Barriuso1, Diego Martín-Sanchez1, Julio M Martinez-Moreno2

  • 1Research Institute-Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain; REDINREN, Madrid, Spain.

Redox Biology
|February 25, 2020
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Summary

Omeprazole, a common acid reflux medication, can cause kidney cell death through oxidative stress. This study shows omeprazole induces dose-dependent tubular cell death, potentially explaining its link to kidney disease.

Keywords:
Cell deathNephrotoxicityOmeprazoleOxidative stressTubular proximal cells

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Area of Science:

  • Nephrology
  • Cell Biology
  • Pharmacology

Background:

  • Omeprazole, a proton pump inhibitor, is linked to chronic kidney disease.
  • The direct toxicity of omeprazole on renal cells remains unclear.
  • Cell death is a critical factor in kidney disease pathogenesis.

Purpose of the Study:

  • To investigate the potential lethal effects of omeprazole on renal tubular cells.
  • To determine if omeprazole induces cell death at concentrations relevant to patient exposure.
  • To elucidate the mechanisms underlying omeprazole-induced renal cell death.

Main Methods:

  • Utilized human and murine proximal tubular cell lines and primary cultures.
  • Assessed cell death using annexin V/7-AAD staining and LDH release.
  • Investigated the roles of oxidative stress, caspases, necroptosis, and ferroptosis.
  • Administered omeprazole parenterally to mice and analyzed kidney tissue markers.

Main Results:

  • Omeprazole induced dose-dependent cell death in proximal tubular cells.
  • Cell death occurred at both high and clinically relevant low concentrations.
  • Omeprazole triggered necrosis, oxidative stress, and mitochondrial/lysosomal dysfunction.
  • N-acetyl-cysteine mitigated omeprazole-induced oxidative stress and cell death, while iron overload exacerbated it.
  • In vivo studies showed increased tubular cell death and renal injury markers (NGAL, HO-1) in mice.

Conclusions:

  • Omeprazole can directly induce renal tubular cell death.
  • Oxidative stress and mitochondrial dysfunction are key mechanisms in omeprazole nephrotoxicity.
  • These findings suggest a cellular basis for the association between omeprazole use and kidney disease.