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/m2 and 1.5 +/- 0.35 years v. 13.8 +/- 0.48 kg/m2 and 2 +/- 0.25 years, respectively). The basal GH concentrations in CRF patients (4.1 +/- 0.8 micrograms/l) were significantly higher than those for the NVSS group (1.56 +/- 0.2 micrograms/l). The peak GH response to clonidine was significantly lower in children with CRF (8.4 +/- 1.7 micrograms/l) v. (19.6 +/- 2.3 micrograms/l) for the control group (P < 0.01). Eight out of the 14 children with CRF did not mount a proper GH response (> 10 micrograms/l) to clonidine stimulation whereas the GH response of all the children with NVSS was above 10 micrograms/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/l). 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.(ABSTRACT TRUNCATED AT 250 WORDS)