The insulin-like growth factor-I axis in acute renal failure

Michael M. Friedlaender, Fernando C. Fervenza, Tanny Tsao, Fay Hsu, Ralph Rabkin

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

We have examined the response of the renal insulin-like growth factor (IGF-I) axis to acute ischemic injury in the rat Key findings included a decrease in IGF-I mRNA and peptide levels, a decrease in GH receptor gene plus protein expression and a decrease in the IGF binding proteins except for IGF binding protein 1. Administration of GH to compensate for the reduced GH receptor binding corrected the IGF-I mRNA levels suggesting a relative GH deficiency. Interestingly, IGF-I receptor mRNA levels were unchanged while plasma membrane IGF-I receptor number increased two fold. This appeared to be due to a redistribution of receptors to a 'membrane location. IGF-I receptor autophosphorylation and tyrosine kinase activity were intact despite severe uremia for up to 6 days. We propose that this increase of functional IGF-I receptors following acute tubular necrosis will sensitize the kidney to the administration of exogenous IGF-I.

Original languageEnglish (US)
Pages (from-to)343-348
Number of pages6
JournalRenal Failure
Volume20
Issue number2
DOIs
StatePublished - Jan 1 1998

Keywords

  • Acute renal failure
  • Insulin-like growth factor

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Nephrology

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