Deficiency of 1,25-dihydroxyvitamin D plays an important role in the pathogenesis of secondary hyperparathyroidism. Adequate replacement of this hormone is required to normalize parathyroid gland function and restore bone homeostasis in patents with advanced renal failure. Controversy exists regarding the best method of administering 1,25-dihydroxyvitamin D. Although intial, uncontrolled clinical trials suggested the superiority of intravenous calcitriol treatment, more recent controlled investigations have shown that different routes (oral versus intravenous), frequency (daily versus intermittent) and dosing (physiologic versus pharmacologic) of calcitriol administration are equivalent. Overall, the response to calcitriol treatment depends more on the severity of secondary hyperparathyroidism and the presence of confounding variables, such as hyperphosphatemia and acquired abnormalities of parathyroid cell function, than on the method of calcitriol administration.