Effect of calcitriol treatment and withdrawal on hyperparathyroidism in haemodialysis patients with hypocalcaemia

Background. Calcitriol is used to treat secondary hyperparathyroidism in di alysis patients. For similarly elevated parathyroid hormone (PTH) levels, t he PTH response to calcitriol treatment is believed to he better in hypocal caemic dialysis patients than in dialysis patients with higher serum calciu m values. Furthermore, few studies have evaluated the rapidity of the rebou nd in serum PTH values after prolonged treatment with calcitriol. Our goal was to evaluate (i) the PTH response to calcitriol treatment in hypocalcaem ic haemodialysis patients, (ii) the rapidity of rebound in PTH after calcit riol treatment was stopped, and (iii) whether the effect of calcitriol trea tment on PTH levels could be separated from those produced by changes in se rum calcium and phosphate values. Methods. Fight haemodialysis patients (29 +/- 3 years) with hypocalcaemia a nd hyperparathyroidism were treated thrice weekly with 2 mug of intravenous calcitriol and were dialysed with a 3.5 mEq/l calcium dialysate. Parathyro id function (PTH-calcium curve) was determined before and after 30 weeks of calcitriol treatment and 15 weeks after calcitriol treatment was stopped. Results, Pretreatment PTH and ionized calcium values were 90 +/- 127 pg/ml and 3.89 +/- 0.12 mg/dl (normal, 4.52 +/- 0.07 mg/dl). During calcitriol tr eatment, one patient did not respond? but basal (predialysis) PTH values in the other seven patients decreased from 846 +/- 129 to 72 +/- 12 pg/ml, P < 0.001 and in all seven patients, the decrease exceeded 85%. During the 15 weeks after calcitriol treatment was stopped, a slow rebound in basal PTH values in the seven patients was observed, 72 <plus/minus> 12 to 375 +/- 44 pg/ml. Covariance analysis was used to evaluate the three tests of parathy roid function (0, 30, and 45 weeks), and showed that calcitriol treatment w as associated with reductions in maximal PTH values while reductions in bas al PTH were affected by ionized calcium and serum phosphate. The basal/maxi mal PTH ratio and the set point of calcium were associated with changes in ionized calcium. Conclusions. In haemodialysis patients with hypocalcaemia, (li) moderate to severs hyperparathyroidism responded well to treatment with calcitriol, (i i) reductions in maximal PTH were calcitriol dependent while reductions in basal PTH were affected by the ionized calcium and serum phosphate concentr ations, (iii) changes in the basal/maximal PTH ratio and the set point of c alcium were calcium dependent, and (iv) the delaved rebound in basal PTH le vels after withdrawal of calcitriol treatment may have been due to the long duration of treatment and the marked PTH suppression during treatment.