Effect of prolonged uremia on insulin-like growth factor-I receptor autophosphorylation and tyrosine kinase activity in kidney and muscle

Tanny Tsao, Fernando Fervenza, Michael Friedlaender, Yu Chen, Ralph Rabkin

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Recently, based on a study in rats with chronic renal failure (CRF), it has been suggested that IGF-I resistance in uremia may be caused in part by defective IGF-I receptor autophosphorylation and tyrosine kinase activity. Thus if such a defect were to develop in prolonged acute renal failure (ARF), this may explain why IGF-I therapy, effective in rats, has failed to promote recovery from ARF in patients. Accordingly, we examined IGF-I receptor function in rats with uremia of increasing duration and in pair-fed sham-operated controls. After 6 days of prolonged ARF, kidney IGF-I receptor binding increased twofold, while IGF-I stimulated receptor phosphorylation and tyrosine kinase activity were unchanged. Muscle receptor binding, autophosphorylation and tyrosin kinase activity were similar to control values after 6 or even 21 days of uremia. Taking all these findings together it appears that IGF-I resistance in uremia cannot be attributed to a receptor defect. This in turn argues against altered receptor function as a cause of the failure of IGF-I to modify clinical ARF.

Original languageEnglish (US)
Pages (from-to)285-292
Number of pages8
JournalExperimental Nephrology
Volume10
Issue number4
DOIs
StatePublished - 2002

Keywords

  • Acute renal failure
  • Chronic renal failure
  • Insulin-like growth factor
  • Receptors
  • Signal transduction
  • Uremia

ASJC Scopus subject areas

  • Nephrology

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