Chronic gentamicin nephrotoxicity: Continued tubular injury with preserved glomerular filtration function

Donald Houghton, D. Lee, D. N. Gilbert, W. M. Bennett

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

After an initial episode of acute tubular necrosis, apparent resistance to gentamicin nephrotoxicity develops in rats during prolonged drug administration. The authors studied this phenomenon by examining the autoradiographic distribution of 3H-gentamicin and 3H-thymidine during 5 weeks of gentamicin treatment and by analyzing renal structure and function after a 12-week course of treatment. These studies show that regenerating cells exclude gentamicin, but concentrate it again after maturation, and that the rate of thymidine incorporation is still high well after recovery from acute toxic injury. After 12 weeks of gentamicin, the glomerular filtration rate was only modestly diminished, whereas in vitro cortical organic ion transport was substantially impaired. Light and electron microscopy demonstrated all phases of injury and recovery among cells of most proximal tubules and evidence of chronic tubulointerstitial disease. It is concluded that 'resistance' to gentamicin is a state of persistent tubular cell injury obscured functionally by preservation of the glomerular filtration rate and histologically by asynchrony of cell necrosis and regeneration.

Original languageEnglish (US)
Pages (from-to)183-194
Number of pages12
JournalAmerican Journal of Pathology
Volume123
Issue number1
StatePublished - 1986

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Gentamicins
Wounds and Injuries
Glomerular Filtration Rate
Thymidine
Necrosis
Poisons
Ion Transport
Regeneration
Electron Microscopy
Chronic Disease
Kidney
Light
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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Chronic gentamicin nephrotoxicity : Continued tubular injury with preserved glomerular filtration function. / Houghton, Donald; Lee, D.; Gilbert, D. N.; Bennett, W. M.

In: American Journal of Pathology, Vol. 123, No. 1, 1986, p. 183-194.

Research output: Contribution to journalArticle

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