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Related Experiment Videos

Aminoglycoside-mediated calciuresis.

W C Elliott1, D S Patchin

  • 1Department of Medicine, State University of New York, Syracuse.

The Journal of Pharmacology and Experimental Therapeutics
|July 1, 1992
PubMed
Summary

Gentamicin administration causes a rapid and significant increase in urinary calcium excretion in rats. This effect, termed gentamicin-induced calciuria, appears related to the drug

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Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Gentamicin and calcium compete for binding sites in renal tissues.
  • Gentamicin exhibits calcium channel blocking properties.
  • In vitro studies show calcium channel blockers reduce calcium uptake in renal cells.

Purpose of the Study:

  • To investigate the acute in vivo effects of gentamicin on renal calcium handling.
  • To determine the relationship between gentamicin administration and urinary calcium excretion.

Main Methods:

  • Intravenous bolus administration of gentamicin (10 mg/kg) to F344 rats.
  • Measurement of fractional calcium excretion, glomerular filtration rate, and urinary electrolytes.
  • Correlation analysis of urinary calcium with gentamicin dose and concentration.

Main Results:

  • Fractional calcium excretion increased dramatically (11% to 128%) within 30 minutes post-gentamicin.
  • Calciuria was dose-related, correlated with pre-administration urinary calcium, and peaked immediately.
  • Urinary calcium normalized within 90 minutes after bolus, but remained high during continuous infusion.
  • Tobramycin induced similar calciuria; verapamil and potassium dichromate did not.

Conclusions:

  • Gentamicin induces acute calciuria in rats, independent of parathyroid function or dietary calcium.
  • The mechanism may involve brush border binding competition, intraluminal calcium channel blockade, or ATPase inhibition.
  • Aminoglycoside-induced calciuria warrants further investigation into its underlying mechanisms and clinical implications.

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