PREVENTION OF HYPERCALCIURIA AND STONE-FORMING PROPENSITY DURING PROLONGED BEDREST BY ALENDRONATE

The bone loss and hypercalciuria induced by immobilization or the decr eased gravitational forces of space are well described. Using a model of bedrest immobilization, the ability of a potent aminobisphosphonate , alendronate, to avert hypercalciuria and stone-forming propensity wa s tested. Sixteen male subjects participated in a randomized, placebo- controlled trial in which they received either 20 mg of alendronate or placebo 2 weeks prior to and during 3 weeks of strict bedrest. Parame ters of bone and calcium metabolism and urinary crystallization of sto ne-forming salts were measured before and at the end of bedrest. In th e placebo group, bedrest increased urinary calcium (209 +/- 47 to 267 +/- 60 mg/day, p < 0.01) and the saturation of calcium phosphate. Befo re bedrest, the alendronate group had a significantly lower serum calc ium (8.8 +/- 0.4 vs. 9.6 +/- 0.5 mg/dl, p < 0.01) and higher serum PTH (62.4 +/- 33.1 vs. 23.1 +/- 7.5 pg/ml, p < 0.01) compared with the pl acebo group. Moreover, the alendronate group had a lower urinary calci um (75 +/- 41 mg/day) and saturation of calcium oxalate and calcium ph osphate. These effects of alendronate were sustained during bedrest. F ollowing bedrest in the alendronate group, urinary calcium rose to 121 +/- 50 mg/day, a value less than that in the placebo group before or during bedrest. Similarly, urinary saturation of calcium oxalate and c alcium phosphate rose with bedrest in the alendronate-treated patients but remained lower than values obtained in placebo-treated patients b efore or during bedrest. Alendronate inhibits bone mineral loss and av erts the hypercalciuria and increased propensity for the crystallizati on of stone-forming calcium salts which occurs during 3 weeks of stric t bedrest.