OBJECTIVE: To study bone density in hypercalciuric patients, when classified according to the main metabolic defect. METHODS: We studied 49 patients, aged 19-60 years with calcium stones and idiopathic hypercalcuria. All subjects underwent an evaluation of mineral metabolism and a spinal and femoral DEXA measurement. Then, patients were classified as having Fasting (FH, 31 subjects) or Absorptive (AH, 18 patients) Hypercalciuria according to a standard oral calcium load. RESULTS: Spinal bone density was lower only in FH patients as compared to controls (p <0.001). Bone alkaline phosphatase and urine hydroxyproline were higher with respect to controls only in patients with FH (p <0.005 and p <0.015, respectively). After low calcium diet, hydroxyproline excretion continued to be higher in FH patients (p <0.05). Although in the normal range, serum and urine uric acid were higher in hypercalciuric subjects (p <0.03 and p <0.005, respectively); blood pH was lower in hypercalciuric patients than in controls (p <0.01). In FH patients urine hydroxyproline negatively correlated with spinal and femoral density (p <0.001 and p <0.005, respectively), and blood pH positively correlated with spinal density. CONCLUSIONS: a disordered bone metabolism and bone loss are present only in patients with fasting hypercalciuria. An excessive acid load, possibly of dietary origin, might be involved as a pathogenetic factor.
OBJECTIVE: To study bone density in hypercalciuric patients, when classified according to the main metabolic defect. METHODS: We studied 49 patients, aged 19-60 years with calcium stones and idiopathic hypercalcuria. All subjects underwent an evaluation of mineral metabolism and a spinal and femoral DEXA measurement. Then, patients were classified as having Fasting (FH, 31 subjects) or Absorptive (AH, 18 patients) Hypercalciuria according to a standard oral calcium load. RESULTS: Spinal bone density was lower only in FHpatients as compared to controls (p <0.001). Bone alkaline phosphatase and urine hydroxyproline were higher with respect to controls only in patients with FH (p <0.005 and p <0.015, respectively). After low calcium diet, hydroxyproline excretion continued to be higher in FHpatients (p <0.05). Although in the normal range, serum and urine uric acid were higher in hypercalciuric subjects (p <0.03 and p <0.005, respectively); blood pH was lower in hypercalciuric patients than in controls (p <0.01). In FHpatients urine hydroxyproline negatively correlated with spinal and femoral density (p <0.001 and p <0.005, respectively), and blood pH positively correlated with spinal density. CONCLUSIONS: a disordered bone metabolism and bone loss are present only in patients with fasting hypercalciuria. An excessive acid load, possibly of dietary origin, might be involved as a pathogenetic factor.
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