HIGH-DOSE ORAL CALCITRIOL AND ZERO CALCIUM PERITONEAL SOLUTIONS IN CAPD PATIENTS WITH REFRACTORY SECONDARY HYPERPARATHYROIDISM

We evaluated the effect of pulse oral calcitriol (4 mu g three times w eekly for 6 months) on parathyroid function in nine CAPD patients with hyperparathyroidism refractory to conventional low-dose oral calcitri ol. Zero calcium peritoneal solutions were used to prevent the develop ment of hypercalcaemia. The peritoneal loss of calcium increased from 168 +/- 40 to 417 +/- 48 mg/day using zero calcium solutions. Pulse or al calcitriol resulted in a significant decrease in PTH (from 617 +/- 272 to 382 +/- 299 pg/ml) by the 15th day of therapy, while serum iCa did not change from baseline. During the first month of therapy the me an PTH levels remained significantly reduced compared to baseline, the reafter PTH increased in four of nine patients. Hyperphosphataemia was not satisfactorily controlled in four patients, despite large amounts of binders used; seven of nine patients developed hypercalcaemia and required either the substitution of calcium acetate for calcium carbon ate or reduction of calcitriol dose. Three patients showed a progressi ve increase in PTH. In conclusion our data suggest that in most CAPD p atients with severe hyperparathyroidism oral calcitriol pulse therapy is not effective in maintaining a permanent suppression in PTH levels.