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Gentamicin causes endocytosis of Na/Pi cotransporter protein (NaPi-2)

V Sorribas1, N Halaihel, K Puttaparthi

  • 1University of Zaragoza, Zaragoza, Spain.

Kidney International
|March 7, 2001
PubMed

Insights

Gentamicin antibiotic impairs kidney phosphate transport by reducing type II sodium-phosphate (Na/Pi) cotransporter protein in proximal tubules. This occurs post-transcriptionally, affecting kidney function.

Area of Science:

  • Nephrology
  • Pharmacology
  • Molecular Biology

Background:

  • Aminoglycoside antibiotics like gentamicin cause renal toxicity, primarily affecting proximal tubular function.
  • Previous studies showed gentamicin impairs sodium gradient-dependent phosphate (Na/Pi) cotransport activity in rat kidneys.

Purpose of the Study:

  • To investigate the molecular mechanisms behind gentamicin-induced impairment of Na/Pi cotransport activity.
  • To determine the specific role of the proximal tubular type II Na/Pi cotransporter in this impairment.

Main Methods:

  • Rats were treated with gentamicin for one, two, or three days.
  • Analyzed Na/Pi cotransporter activity and protein abundance in brush-border membranes (BBM) from superficial and juxtamedullary cortices.
  • Utilized Western blot, immunofluorescence microscopy, and Northern blot analyses.

Main Results:

  • Gentamicin progressively decreased Na/Pi cotransporter activity and protein abundance in superficial cortical BBM.
  • Protein levels decreased by 50%, 63%, and 83% after one, two, and three days of treatment, respectively.
  • No changes were observed in juxtamedullary cortex BBM; protein accumulated in endosomes/lysosomes, and mRNA levels remained unaffected.

Conclusions:

  • Gentamicin inhibits Na/Pi cotransport activity by reducing type II Na/Pi cotransporter protein expression in the proximal tubular apical BBM.
  • The observed inhibition is likely mediated by post-transcriptional mechanisms, as mRNA levels were not reduced.
Abstract

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