Abstract
Insulinlike growth factor I (IGF-I), IGF-I receptors, and IGF-binding proteins are expressed in different segments of the nephron in a relationship that suggests autocrine, paracrine, and endocrine modes of action. IGF-I contributes to compensatory nephron growth in a variety of experimental renal diseases with loss in functioning nephron number, and to tissue repair after ischemic acute tubular necrosis. IGF-I causes arteriolar dilatation in the kidney and increases the glomerular filtration rate in experimental animals, in normal subjects, as well as in patients with chronic renal failure, and this effect of the peptide is probably mediated by nitric oxide. IGF-I raises proximal tubular phosphate reabsorption and may increase sodium absorption in distal tubules. In the nephrotic syndrome, IGF-I- and IGF-binding protein complexes are excreted in urine and IGFBP-3 protease activity is increased, causing complex abnormalities in the IGF-system.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
