Oral phosphate load unmasks underlying renal phosphate leak in symptomatic and asymptomatic members of family with idiopathic hypercalciuria.

The effects of a 2 Gm oral phosphorus load in a family with idiopathic hypercalciuria (IH) consisting of 3 symptomatic (DT, CS, DS) and 2 asymptomatic (MS, PD) members were compared with 12 normal control subjects. Biochemical parameters measured included: total and ionized calcium, phosphorus, intact and carboxyl-terminal parathyroid hormone, urinary calcium, phosphorus, and sodium. Water loading had no effect on these parameters. After the phosphorus load, serum phosphorus rose 1.60 mg/dl in the control subjects but only 1.34 mg/dl in the IH family at the end of one hour. Basal tubular reabsorption of phosphate (TRP) were comparable in the control subjects and the IH family. After the phosphorus load, the TRP in the control subjects fell (average 9.2%) accompanied by a significant (P less than 0.02) rise in the carboxyl-terminal parathyroid hormone. Except for DT who had been taking hydrochlorothiazide, the TRP fell dramatically in the rest of the IH family (DS 25%, CS 12%, PD 26%, MS 50%) in the absence of any perturbations in either the intact or carboxyl-terminal parathyroid hormone. A hypocalciuric effect was observed in the IH family but not in the control subjects after phosphorus loading. The oral phosphorus challenge unmasked a parathyroid hormone independent renal phosphate leak in both symptomatic and asymptomatic members in a family with idiopathic hypercalciuria.