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Glomerular permeability to macromolecules in gentamicin-treated rats.

M L de-Barros-e-Silva1, W A Varanda, J J Lachat

  • 1Departamento de Fisiologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Brasil.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|January 1, 1992
PubMed
Summary

Gentamicin treatment significantly increased albuminuria in rats, indicating heightened glomerular permeability to negatively charged proteins. This suggests potential kidney filter damage from gentamicin exposure.

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Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Gentamicin is a common antibiotic with known nephrotoxic potential.
  • The glomerular barrier's integrity is crucial for kidney function.
  • Understanding gentamicin's specific effects on glomerular permeability is important for patient safety.

Purpose of the Study:

  • To investigate the impact of gentamicin on the functional properties of the rat glomerular barrier.
  • To assess changes in glomerular permeability to macromolecules following gentamicin administration.

Main Methods:

  • Wistar rats were administered gentamicin (80 mg/kg/day) for 6 days.
  • Albuminuria was measured on days 1, 3, and 5.
  • Glomerular permeability to neutral dextrans and albumin was evaluated on day 6 using electron microscopy and clearance studies.

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Main Results:

  • Gentamicin treatment led to a significant increase in albuminuria (from 74 µg/24h to 11.5 mg/24h).
  • Albumin was detected within the glomerular filter and proximal tubular cells.
  • Fractional clearances of neutral dextrans (18-41 Å) remained unchanged, suggesting selective permeability changes.

Conclusions:

  • Gentamicin increases glomerular permeability to negatively charged macromolecules like albumin in rats.
  • This effect is likely due to the interaction of gentamicin, a polycation, with negative charges on the glomerular filter.
  • The findings highlight a specific mechanism of gentamicin-induced kidney injury affecting glomerular filtration.