Effect of oral calcium loading on intact PTH and calcitriol in idiopathic renal calcium stone formers and healthy controls

Abstract

Abstract. The calciuric response after an oral calcium load (lOOOmg elemental calcium together with a standard breakfast) was studied in 13 healthy male controls and 21 recurrent idiopathic renal calcium stone formers, 12 with hypercalciuria (U Ca x V>7.50 mmol/24h) and nine with normocalciuria. In controls, serum 1,25(OH) 2 vitamin D3 (calcitriol) remained unchanged 6 h after oral calcium load (50.6 + 5.1 versus 50.9 + 5.0 pg/ml), whereas it tended to increase in hypercalciuric (from 53.6 + 3.2 to 60.6 + 5.4 pg/ml, P = 0.182) and fell in normocalciuric stone formers (from 45.9 + 2.6 to 38.1+3.3 pg/ml, P = 0.011). The total amount of urinary calcium excreted after OCL was 2.50 + 0.20 mmol in controls, 2.27 + 0.27 mmol in normocalciuric and 3.62 + 0.32 mmol in hypercalciuric stone formers (P = 0.005 versus controls and normocalciuric stone formers respectively); it positively correlated with serum calcitriol 6h after calcium load (r = 0.392, P=0.024). Maximum increase in urinary calcium excretion rate, ACa-E max , was inversely related to intact PTH levels in the first 4 h after calcium load, i.e. more pronounced PTH suppression predicted a steeper increase in urinary calcium excretion rate. Twenty-four-hour urine calcium excretion rate was inversely related to the ratio of A calcitriol/APTH max after calcium load (r = -0.653, P = 0.0001), indicating that an abnormally up-regulated synthesis of calcitriol and consecutive relative PTH suppression induce hypercalciuria. Finally, late absorption of calcium as suggested by maximum urinary calcium excretion beyond 4 h after oral calcium load was as rare in hypercalciuric stone formers (2 of 12) as in controls (1 of 13) and did not occur in normocalciuric stone formers.