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Pulse Calcitriol Therapy

Despite extensive experience with calcitriol in managing the secondary hyperparathyroidism of chronic renal failure (1-3), reproducibly effective treatment is not always assured. Calcitriol is very effective in correcting uremic-induced hypocalcemia but less reliable in suppressing PTH secretion and ameliorating renal osteodystrophy in certain settings. Such complicating problems as hyperphosphatemia and hypercalcemia frequently limit the dose of calcitriol and contribute to the failure of calcitriol to cause regression of parathyroid gland size. Hyperphosphatemia, resulting mainly from inadequate dietary control, is exacerbated by calcitriol-induced phosphate absorption and phosphate egress from bone (4). Hypercalcemia is also a major concern since calcium-containing phosphate binders have become accepted therapy for control of phosphate absorption. Even though lowering the dialysate calcium concentration to 2.5 mEq/L has reduced the number of hypercalcemic episodes in patients receiving calcitriol (3, careful monitoring of calcitriol dose continues to be necessary. Generally, low oral doses of calcitriol (0.25-0.5 pg/day) are effective in reducing serum PTH when levels are elevated in association with hypocalcemia (1, 6, 7). Hypocalcemia is the major stimulus for hypersecretion of parathyroid cells and is more prevalent in the final stages of renal failure and during the initial time of dialysis. With increasing time on dialysis, elevated PTH levels are more often associated with normal or elevated serum calcium, indicating the presence of significant parathyroid cell hyperplasia. In many long-term dialysis patients, elevated PTH levels are more refractory to daily oral calcitriol; long-term intravenous calcitriol has proven to be effective in substantially reducing these levels and the hormone’s effect on bone (8,9). Unfortunately, for intravenous calcitriol to be effective in this setting, prolonged therapy (>1 year) is usually required, which adds to the cost of an already expensive drug. Why does intravenous calcitriol suppress PTH secretion in patients refractory to oral calcitriol? Suppression likely occurs because the higher circulating levels of 1,25-dihydroxyvitamin D induced by this method of administration (10) are sufficient to