Treatment of Secondary Hyperparathyroidism by Intravenous Calcitriol

Abstract

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 in the high parathyroid hormone (PTH) levels of these patients (1, 2). Thus, it is not surprising that the administration of calcitriol orally (3, 4) has resulted in the amelioration or even dramatic improvement of secondary hyperparathyroidism. What makes the use of intravenous calcitriol an attractive modality of therapy is the recent observation that calcitriol per se, in the absence of hypercalcemia inhibit both synthesis and secretion of PTH (5, 6). In the present chapter we will briefly review the physiological action of calcitriol in dialysis patients in regard to divalent ion metabolism, then we will discuss new data on calcitriol and PTH interaction and finally, the available clinical data on the intravenous use of calcitriol will be reviewed.