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Heat shock protein 70 induction and its urinary excretion in a model of acetaminophen nephrotoxicity

Sara M Molinas1, Marina Rosso, Nahuel Z Wayllace

  • 1Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Rosario, Argentina.

Pediatric Nephrology (Berlin, Germany)
|March 31, 2010
PubMed

Insights

Acetaminophen (APAP) overdose can harm kidneys. N-acetyl-beta-D glucosaminidase (NAG) in urine signals early kidney damage, while heat shock protein 70 (HSP70) in urine indicates kidney injury and tubule integrity loss.

Area of Science:

  • Toxicology
  • Biochemistry
  • Nephrology

Background:

  • Acetaminophen (APAP) is a common analgesic-antipyretic medication.
  • APAP overdose can lead to significant kidney toxicity (nephrotoxicity).
  • Early detection of APAP-induced nephrotoxicity is crucial for timely intervention.

Purpose of the Study:

  • To investigate the induction of heat shock protein 70 (HSP70) in the kidney following APAP administration.
  • To determine if HSP70 can be detected in urine as a biomarker of APAP nephrotoxicity.
  • To evaluate N-acetyl-beta-D glucosaminidase (NAG) as an early biomarker for APAP-induced kidney injury.

Main Methods:

  • An in vivo model of APAP-induced nephrotoxicity was established in male Wistar rats.
  • Rats received a toxic dose of APAP (1,000 mg/kg body weight i.p.).
  • Renal function (urea, creatinine), histological changes, cellular injury (Na+/K+ ATPase solubility), glutathione levels, and urinary NAG excretion were assessed. HSP70 levels in urine and renal cortex were measured.

Main Results:

  • Urinary NAG excretion significantly increased at 4 hours post-APAP administration, preceding significant changes in urea and creatinine levels.
  • Histological alterations were mild at 4 hours but resolved by 48 hours.
  • HSP70 was detected in urine from 4 to 24 hours and its abundance increased in the renal cortex.
  • No significant differences in renal function markers or NAG excretion were observed between control and APAP-treated groups at 48 hours.

Conclusions:

  • Urinary NAG is a sensitive early biomarker for detecting APAP-induced nephrotoxicity.
  • Urinary HSP70 detection, alongside renal HSP70 induction, suggests tubule damage and can serve as a marker of APAP nephrotoxicity.
  • These findings highlight potential urinary biomarkers for monitoring kidney injury following acetaminophen overdose.

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