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Insulin-like growth factor I in the kidney
1Division of Nephrology and Hypertension, Harbor-UCLA Medical Center, Torrance 90509, USA.
Insulin-like growth factor I (IGF-I) is synthesized in renal glomeruli and distal tubules. The rather high serum IGF-I levels (20-40 nM) result mainly from synthesis in the liver. In the circulation > or = 99% of IGF-I is bound in binding protein complexes. IGF-I can act in the kidney by autocrine and paracrine as well as endocrine modes. IGF-I raises GFR through reducing arteriolar resistance and increasing LpA. The peptide also increases the tubule transport of phosphate both in vitro and in vivo. IGF-I has been associated with the initiation of hypertrophy in models of compensatory renal growth and may contribute to the accumulation of extracellular matrix proteins in the nephron in chronic renal diseases. In the nephrotic syndrome, IGF-I is ultrafiltered into tubule fluid in association with IGF-binding protein-2 and activates apical proximal tubule cell receptors.
Insulin-like growth factor I (IGF-I) is synthesized in renal glomeruli and distal tubules. The rather high serum IGF-I levels (20-40 nM) result mainly from synthesis in the liver. In the circulation > or = 99% of IGF-I is bound in binding protein complexes. IGF-I can act in the kidney by autocrine and paracrine as well as endocrine modes. IGF-I raises GFR through reducing arteriolar resistance and increasing LpA. The peptide also increases the tubule transport of phosphate both in vitro and in vivo. IGF-I has been associated with the initiation of hypertrophy in models of compensatory renal growth and may contribute to the accumulation of extracellular matrix proteins in the nephron in chronic renal diseases. In the nephrotic syndrome, IGF-I is ultrafiltered into tubule fluid in association with IGF-binding protein-2 and activates apical proximal tubule cell receptors.