Growth hormone metabolism in uremia.

Abstract

The influence of chronic renal failure (CRF) on growth hormone (GH) and insulin-like growth factor I (IGF-I) metabolisms is not well understood. Clinical studies on GH secretion in CRF have yielded conflicting results. In vitro, pituitary GH secretion has been shown to be unimpaired in moderate uremia. CRF reduces binding of GH to liver as a result of decreased number of GH receptors. CRF induces elevation of serum GH concentrations and does not modify the circulating values of IGF-I. However, the somatomedin bioactivity of uremic serum is depressed, and unsaturated low-molecular-weight IGF-I-binding proteins have been suggested to act as inhibitory factors of IGF-I action. Circulating GH and IGF-I do not necessarily reflect the state of GH and IGF-I in tissues, and further investigations on the effect of CRF on GH and IGF-I metabolisms at the growth plate level are clearly required.