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Effects of renal failure on the growth hormone-insulin-like growth factor axis
1Clinical Care Center, Texas Children's Hospital, Houston 77030, USA.
Insights
Children with chronic renal failure (CRF) experience growth failure due to abnormal growth hormone-insulin-like growth factor (GH-IGF) axis. Growth hormone (GH) therapy improves growth by increasing IGF bioactivity through the 150 kd serum ternary complex.
Area of Science:
- Pediatric Endocrinology
- Nephrology
- Growth Factor Biology
Background:
- Children with chronic renal failure (CRF) often exhibit growth retardation.
- Abnormalities in the growth hormone-insulin-like growth factor (GH-IGF) axis are implicated in CRF-related growth failure.
- Serum GH and IGF levels are normal, but IGF bioactivity is reduced due to excess IGF binding proteins (IGFBPs).
Purpose of the Study:
- To investigate the impact of growth hormone (GH) therapy on the GH-IGF axis in children with CRF.
- To elucidate the mechanisms by which GH influences IGF bioactivity and growth in this population.
Main Methods:
- Analysis of serum GH, IGF, and IGF binding protein (IGFBP) levels in children with CRF before and after GH treatment.
- Characterization of IGFBPs in different serum fractions (35 kd and 150 kd ternary complex).
Main Results:
- GH treatment in children with CRF led to catch-up growth.
- Catch-up growth correlated positively with increased components of the 150 kd serum ternary complex (acid-labile subunit, IGFBP-3, IGF-I, IGF-II).
- GH therapy increased IGFBP-3 within the 150 kd complex, enhancing IGF bioactivity and potentially overcoming inhibitory IGFBPs in the 35 kd fraction.
Conclusions:
- Growth hormone (GH) therapy appears to enhance the 150 kd serum ternary complex in children with CRF.
- Increased IGFs released from the ternary complex may promote growth by counteracting the inhibitory effects of excess IGFBPs.
- This mechanism offers a potential therapeutic strategy for growth failure in pediatric chronic renal failure.
Abstract:
Children with chronic renal failure (CRF) often have retarded growth, and abnormalities of the growth hormone-insulin-like growth factor (GH-IGF) axis in CRF may contribute to this growth failure. The serum GH and IGF levels are normal in these children, but IGF bioactivity is low as a result of excess IGF binding proteins (IGFBPs) in the 35 kd serum fractions. The levels of intact IGFBP-1, -2, and -6 and of a 29 kd IGFBP-3 fragment are all high, and the IGFBP-1 and -2 levels correlate negatively with height. Children with CRF who are treated with GH show catch-up growth that correlates positively with the increase in each component of the 150 kd serum ternary complex (acid-labile subunit, IGFBP-3, IGF-I, and IGF-II). Consistent with this observation, the increase in IGFBP-3 levels is confined to the 150 kd serum fractions. Serum levels of IGFBP-1, -2, and -6 do not rise, but serum IGF bioactivity does. Thus GH appears to induce an increase in the ternary complex in the serum of children with CRF. It is possible that IGFs released by the 150 kd serum complex promote growth by overcoming the inhibitory effects of excess IGFBPs in the 35 kd serum fractions.
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