Aquiles Jara

Studies in a hemodialysis patient indicating that calcitriol may have a direct suppressive effect on bone

Calcitriol putatively suppresses bone activity by decreasing parathyroid hormone (PTH) levels. Results of studies in a 52-year-old female maintenance hemodialysis patient suggest that calcitriol may also have a direct suppressive effect on bone. The PTH-calcium relationship was evaluated through the use of low (1 mEq/l) and high (4 mEq/l) calcium hemodialyses that were performed before the initiation of calcitriol treatment, at the end of 6 weeks of thrice-weekly intravenous calcitriol administration, and 6 weeks after the discontinuation of calcitriol. During the low-calcium dialysis, serum calcium decreased more rapidly and to a greater magnitude after calcitriol treatment despite no appreciable difference in basal and maximally stimulated PTH levels; during the high-calcium dialysis, calcitriol treatment resulted in a more rapid increase in serum calcium despite no appreciable difference in basal and maximally suppressed PTH levels. Discontinuation of calcitriol resulted in responses to the low and high calcium dialyses that were similar to those observed before calcitriol treatment. In conclusion, the results suggest that calcitriol may have a direct suppressive effect on bone that is independent of PTH.

Treatment of Secondary Hyperparathyroidism in Maintenance Hemodialysis Patients by Intravenous Calcitriol

Secondary hyperparathyroidism resulting in osteitis fibrosa is the most common bone abnormality observed in dialysis patients. Most recent data strongly suggest that a deficit of calcitriol is an important factor inducing the high parathyroid hormone (PTH) levels observed in these patients (1-2). Thus, it is not surprising that in initials studies the administration of calcitriol orally (3-4) has resulted in the amelioration or even dramatic improvement of secondary hyperparathyroidism. What makes the use of calcitriol an attractive modality of therapy is the recent observation that calcitriol per se, in the absence of hypercalcemia, inhibits both synthesis and secretion of PTH (5-6). In the present discussion, we will briefly review the physiological action of calcitriol in dialysis patients in regard to divalent ion metabolism. Then we will discuss recent data on the interaction of calcitriol and PTH; and finally, the available clinical data on the intravenous use of calcitriol will be reviewed.