Hirschberg R
Division of Nephrology and Hypertension, Harbor-UCLA Medical Center, Torrance 90509, USA.
Miner Electrolyte Metab. 1996;22(1-3):128-32.
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.
胰岛素样生长因子I（IGF-I）在肾小球和远端小管中合成。血清IGF-I水平相当高（20 - 40 nM），主要源于肝脏的合成。在循环中，≥99%的IGF-I与结合蛋白复合物结合。IGF-I可通过自分泌、旁分泌以及内分泌方式在肾脏发挥作用。IGF-I通过降低小动脉阻力和增加LpA来提高肾小球滤过率（GFR）。该肽在体外和体内均能增加肾小管对磷酸盐的转运。在代偿性肾脏生长模型中，IGF-I与肥大的起始有关，并且可能在慢性肾脏疾病中导致肾单位细胞外基质蛋白的积聚。在肾病综合征中，IGF-I与IGF结合蛋白-2一起被超滤入小管液，并激活近端小管顶端细胞的受体。
