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 h ormone (TSH) concentrations, basal (8-6) as well as adrenocorticotroph ic hormone (ACTH) provoked cortisol secretion in 14 prepubertal childr en suffering from chronic renal failure (CRF) with impaired statural g rowth [growth velocity (GV)=3.7+/-0.3 cm/year] and compared these valu es with those of 10 normal age matched children with normal variant sh ort stature (NVSS) (GV=4.6+/-0.4 cm/year). The body mass indices and t he 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 mu g/l) were significantly higher than those for the NVSS group (1.56/-0.2 mu g/l). The peak GH response to clonidine was significantly low er in children with CRF (8.4+/-1.7 mu g/l) v. (19.6+/-2.3 mu g/l) for the control group (P<0.01), Eight out of the 14 children with CRF did not mount a proper GH response (>10 mu g/l) to clonidine stimulation w hereas the GH response of all the children with NVSS was above 10 mu g /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). Howev er, the difference was not statistically significant. There was no sig nificant difference in the FT4, TSH as well as basal (8-h) and ACTH-st imulated cortisol concentrations between the two groups. These data sh ow defective GH release in response to clonidine in children with CRF and suggest the participation of an intrinsic abnormality of the hypot halamic-pituitary growth axis in the aetiology of growth failure in th ese children.