VERTEBRAL DENSITY IN HYPERCALCIURIC LITHIASIS - RELATIONSHIP WITH CALCIUM AND PROTEIN CONSUMPTION AND VITAMIN-D METABOLISM

Forty-two patients with calcium calculi were selected based on calciuria > 0.1 mmol/kg/d on an uncontrolled diet. To measure excretion of sodium, calcium, phosphates and hydroxyproline, a 24-hr urine sample was collected on the 4th day of a milk product-free diet, a fasting urine specimen was collected on the morning of the 5th day and another sample was taken 4 hr after the oral administration of calcium. On the 5th day, plasma levels of calcium, phosphates, intact parathyroid hormone (PTH), calcidiol and calcitriol were determined on an empty stomach and after administration of a calcium load. The results, compared to those of healthy subjects evaluated under the same conditions, enabled classification of the stone-formers as having dietary hypercalciuria (n = 18), when calciuria returned to normal on a low calcium diet, and idiopathic hypercalciuria (n = 24), when the urinary calcium level remained high. Patients with idiopathic hypercalciuria were then classified, according to Pak's criteria, as having absorptive hypercalciuria (n = 8), when the fasting calciuric levels was normal, renal hypercalciuria (n = 1), when fasting hypercalciuria with elevated circulating PTH was controlled by a calcium load, or undetermined hypercalciuria (n = 15) for those individuals with fasting hypercalciuria and normal plasma PTH levels. In addition, vertebral density was measured tomodensitometrically and expressed as a percentage of the normal as a function of sex and age based on a regression line calculated with the results of 239 normal subjects. Results and conclusions : a) vertebral density was normal in dietary hypercalciuria, but decreased in idiopathic hypercalciuria (69 +/- 4%), with no difference between the two subgroups of idiopathic disease ; based on these observations, a distinction can be made between dietary and idiopathic hypercalciurias, but not the subclasses of the latter as defined by Pak ; b) bone hyperresorption seems to explain idiopathic hypercalciuria because fasting calciuria values in these patients were positively correlated with hydroxyproline and negatively correlated with bone density; c) high consumption of non-dairy proteins can favor bone hyperresorption because urea excretion in idiopathic hypercalciuria, higher than in dietary hypercalciuria or normal controls, was correlated with calcium and hydroxyproline excretion, d) calcitriol levels were increased in dietary, and idiopathic hypercalciuria ; this compound seems to have a protective effect on bone in iodiopathic hypercalciuria because high levels were positively correlated with vertebral density and negatively correlated with fasting calciuria ; e) the normal phosphatemia found in idiopathic hypercalciuria, the positive correlation between plasma calcitriol and calcidiol levels and the negative correlation between circulating calcitriol and phosphatemia suggest hypersensitivity of 25(OH) vitamin 1) 1-alpha-hydroxylase to phosphatemia variations within the normal range f) in therapeutic terms, these findings suggest that intake of non-dairy proteins should be limited but not that of milk products which would induce calcium deficiency and thereby favor bone demineralization.