Gestational hypercalciuria causes pathological urine calcium oxalate supersaturations

Gestational hypercalciuria causes pathological urine calcium oxalate supersaturations. Although normal pregnant women are more hypercal-ciuric than women with calcium oxalate nephrolithiasis (243 ± 23 mg/day vs. 194 ± 5 mg/day), pregnancy is not an established stone-forming state and pregnant women do not exhibit pathological crystalluria. One hypothesis to explain their lack of overt stone formation and pathological crystalluria is that pregnancy does not raise urine supersaturation with respect to stone forming salts such as calcium oxalate or calcium monohydrogen phosphate (brushite) to levels as high as in stone forming women. To test this hypothesis, we studied eleven normal women during each trimester of pregnancy, and between six and eight weeks post-partum. During pregnancy, hypercalciuria occurs with unchanged urine volume, citrate and magnesium excretions do not increase proportionally with calcium excretion, and urine pH increases. Supersaturations with respect to calcium oxalate (CaOx) and brushite (Br) are as high as those of women with calcium nephrolithiasis. The lack of pathological crystalluria and stones during pregnancy is not due to a failure of supersaturations to increase; urinary potential for crystallization is as high as in patients with established stone disease