While LS BMD stabilizes after RT, there is a continuing loss of WB and FN BMD. The major causes of bone loss are steroid therapy and continuing PTH, with no tendency towards spontaneous resolution. Increased vitamin D and calcium therapy should be considered for this patient group, and more aggressive therapy, e.g. parathyroidectomy given for patients with resistant PTH of >150 ng/L.

The major threats to bone mass after renal transplantation appear to be ongoing hyperparathyroid bone disease, low renal function, acidosis, systemic disease and hypo-vitaminosis D.

No abstract

The effect of intravenous 1α(OH)D₃ on circulating intact parathyroid hormone (PTH) and COOH-terminal immunoreactive PTH was examined in 21 patients on chronic hemodialysis. The patients were treated for 3 months with increasing doses of 1α(OH)D₃ under careful control of serum Ca²⁺. 1α(OH)D₃ was given intravenously at doses of up to 4 μg three times a week, and blood samples were obtained every week, including 1 week before treatment (basal control). No patients were treated with oral vitamin D metabolites. At the end of the study intact PTH levels were reduced by an average of 67 ± 6%, and COOH-terminal immunoreactive PTH levels were reduced by 35 ± 6%. Serum Ca²⁺ was kept within normal levels, but showed a slight increase from 1.17 to 1.30 rnmol/l. An effect of calcium on PTH secretion could not be excluded, but an effect of 1α(OH)D₃, independent of serum Ca²⁺ was also found. This effect may be mediated by 1,25(OH)₂D₃, assuming a large capacity of the 25-hydroxylase in the liver to convert 1α(OH)D₃ to 1,25(OH)₂D₃. Also, the parathyroid glands may possess receptors for 1α(OH)D₃ with an effect similar to that established for the 1,25(OH)₂D₃ receptors. Thus, although the exact mechanisms ofthe action of 1α(OH)D₃ have not yet been completely clarified, it is concluded that intravenous administration of 1α(OH)D₃ may be of benefit in the treatment of secondary hyperparathyroidism of uremia.