Prevention of hypercalciuria and stone‐forming propensity during prolonged bedrest by alendronate

The bone loss and hypercalciuria induced by immobilization or the decreased 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 was 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. Parameters of bone and calcium metabolism and urinary crystallization of stone‐forming salts were measured before and at the end of bedrest. In the placebo group, bedrest increased urinary calcium (209 ± 47 to 267 ± 60 mg/day, p < 0.01) and the saturation of calcium phosphate. Before bedrest, the alendronate group had a significantly lower serum calcium (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 placebo group. Moreover, the alendronate group had a lower urinary calcium (75 ± 41 mg/day) and saturation of calcium oxalate and calcium phosphate. These effects of alendronate were sustained during bedrest. Following 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 calcium phosphate rose with bedrest in the alendronate‐treated patients but remained lower than values obtained in placebo‐treated patients before or during bedrest. Alendronate inhibits bone mineral loss and averts the hypercalciuria and increased propensity for the crystallization of stone‐forming calcium salts which occurs during 3 weeks of strict bedrest.