Defective Clonidine-induced Growth Hormone Secretion and Normal Thyroid and Adrenal Functions in Prepubertal Children with Chronic Renal Insufficiency (CRF)

We evaluated clonidine-induced growth hormone (GH) secretion, insulin-like factor-I (IGF-I), free thyroxine (FT4), and thyroid stimulating hormone (TSH) concentrations, basal (8-h) as well as adrenocorticotrophic hormone (ACTH) provoked cortisol secretion in 14 prepubertal children suffering from chronic renal failure (CRF) with impaired statural growth [growth velocity (GV)=3.7±0.3 cm/year] and compared these values with those of 10 normal age matched children with normal variant short stature (NVSS) (GV = 4.6 ± 0.4 cm/year). The body mass indices and the bone age delay did not differ between the two groups (14.8 ± 0.7 kg/m 2 and 1.5 ± 0.35 years v. 13.8 ± 0.48 kg/m 2 and 2 ± 0.25 years, respectively). The basal GH concentrations in CRF patients (4.1 ± 0.8 μg/l) were significantly higher than those for the NVSS group (1.56 ± 0.2 μg/l). The peak GH response to clonidine was significantly lower in children with CRF (8.4 ± 1.7 μg/l) v. (19.6 ± 2.3 μg/l) for the control group (P 10 μg/l) to clonidine stimulation whereas the GH response of all the children with NVSS was above 10 μg/l. IGF-I concentrations were higher in patients with CRF (35.6 ± 10.9 IU/l) compared to those for the NVSS group (22.1 ± 4.9 IU/I). However, the difference was not statistically significant. There was no significant difference in the FT4, TSH as well as basal (8-h) and ACTH-stimulated cortisol concentrations between the two groups. These data show defective GH release in response to clonidine in children with CRF and suggest the participation of an intrinsic abnormality of the hypothalamic-pituitary growth axis in the aetiology of growth failure in these children.