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      Effect of Prolonged Uremia on Insulin-Like Growth Factor-I Receptor Autophosphorylation and Tyrosine Kinase Activity in Kidney and Muscle

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          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.

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          Growth hormone, the insulin-like growth factor system, and the kidney

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            Evidence for two insulin-like growth factor I receptors with distinct primary structure that are differentially expressed during development


              Author and article information

              Nephron Exp Nephrol
              Cardiorenal Medicine
              S. Karger AG
              27 June 2002
              : 10
              : 4
              : 285-292
              Research Service Veterans Affairs Palo Alto Health Care System and Departments of Medicine, Stanford University, Palo Alto, Calif., USA
              63703 Exp Nephrol 2002;10:285–292
              © 2002 S. Karger AG, Basel

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              Figures: 6, References: 28, Pages: 8
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