Dialysis Bone Disease in Childhood: Treatment with 25-Hydroxycholecalciferol

Abstract

Summary months of the study; then, the dose was increased to 125 nmole (50 pg) daily duringthe next 5 months. During the study. calcium The effect of 8 months of administration of moderate doses of supp~ements and D2 were d~scont~nued, ~h~ 25hydroxycholecakiferol (25 OH D3) on radiolobic. biolobic. and hydroxide was followed at the same d o w No patient was receiving bone histologic changes was assessed in five children on chronic a n t~c o n v u~s~v a n l drugs, hemodialysis. Osteomalacia, defined by an increase in the thickness index of the osteoid seams and d k r e a s e of the calcification rate, was present on the initial bone biopsy of only one patient and improved with the treatment. Secondary hyperparathyroidism and its prints on bone tissue, noted in all five children, did not improve in the absence of adequate serum phosphorus control. Furthermore, cancellous bone volume diminished in two patients with the administration of 25 OH D3. This activity of the drug could be related to its inhibitory effect of osteoblastic apposition as demonstrated by the decrease in the calcification rates. while the thickness index of the osteoid seams remains normal.Despite the small number of patients studied, these results suggest the importance of limiting the prescription of 25 OH D3 to children suffering from renal osteodystrophy only after having assessed unequivocally an osteomalacic component by histodynamical criteria. Secondary hyperparathyroidism appears not to be improved with moderate doses of 25 OH D3 in the absence of adequate serum phosphorus control.