Skeletal Effects of Growth Hormone and Calcitriol in Children with ESRD

Abstract 1968 Nephrology Platform, Sunday, 5/2

Recombinant human growth hormone (rhGH) and calcitriol (1,25D) are widely utilized to promote linear growth in children with chronic renal failure, but little is known about the respective roles of these hormones as modifiers of bone and mineral metabolism. Thus, 33 pts undergoing peritoneal dialysis were randomly assigned to rhGH (GH) therapy, 0.05 mg/kg/day SQ or to the control (C)group. Measurements of height and biochemical data were obtained monthly. Iliac crest bone biopsy with double tetracycline labeling was done before and after the 9 month study period. Patients with biopsy-proven secondary hyperparathyroidism (2°HPT) were given intraperitoneal 1,25D 1 µg 3×/wk. Data from 22 pts, aged 10.1±1.1 (SE) yrs, who have completed at least 6 months of the study were analyzed. Each group consisted of 11 subjects. Baseline serum Ca and P levels did not differ between groups but serum Alk P, PTH and IGF-1 levels were higher in C than in GH (see table). During combined rhGH and 1,25D therapy, serum Ca levels decreased whereas serum P, Alk P, PTH and IGF-1 levels increased. In contrast, serum AlkP, PTH and IGF-1 levels declined in control subjects given 1,25D alone. This disparity between groups was seen despite progressive increases in the dose of 1,25D in both groups. Initial and final BFR were 362±160 and 566±183 µm²/mm²/day, NS, respectively, in GH, whereas corresponding values were 952±387 and 534±105 µm²/mm²/day, NS in C. Baseline and final BFR correlated with serum PTH levels in C, but this relationship was not demonstrated on follow-up biopsy during combined GH and 1,25 D therapy. Annualized growth velocity did not differ between groups, 5.8±1.0 (C) vs 7.8±0.9 (GH) but the change in SDS for height was higher in GH than in C, 0.34±0.11 vs -0.03±0.11, p<0.05. These results suggest that GH modifies the skeletal response to calcitriol therapy. The optimal dose of 1,25D remains to be defined during GH therapy in pediatric patients with ESRD.

Table 1 No caption available