Orthophosphate Therapy Decreases Urinary Calcium Excretion and Serum 1,25-Dihydroxy Vitamin D Concentrations in Idiopathic Hypercalciuria
The term “idiopathic hypercalciuria” is used to describe the single metabolic abnormality detected by routine laboratory investigation in approximately one-half of the patients who present with idiopathic calcium urolithiasis1. At least two advances have helped our understanding of this disorder; first, is the realization that idiopathic hypercalciuria is not one single entity and more likely, encompasses multiple disorders with separate etiologies. Currently, at least two processes have been identified and idiopathic hypercalciuria is classified as either absorptive or renal hypercalciuria depending on whether increased urinary excretion of calcium is the direct result of intestinal hyperabsorption of calcium, i.e. absorptive hypercalciuria, or impaired renal tubular reabsorption of calcium, i.e. renal hypercalciuria2. A second advance is the finding of increased plasma 1,25-dihydroxy vitamin D levels in some patients with idiopathic hypercalciuria3. The metabolite, 1,25-hydroxy vitamin D, stimulates the intestinal absorption of calcium. Indeed, intestinal hyperabsorption of calcium is present in patients with both absorptive and renal hypercalciuria. Presumably, this increase in plasma 1,25-dihydroxy vitamin D reflects increased synthesis of this hormone by the renal enzyme 25-hydroxy vitamin D-l-α hydroxylase. Experimentally, the activity of this enzyme is increased as a consequence of both increased parathyroid hormone activity4 and with dietary phosphate deprivation5.
KeywordsUrinary Calcium Excretion Idiopathic Hypercalciuria Dietary Phosphate Renal Tubular Reabsorption Calcium Renal Lithiasis
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