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Orthophosphate Therapy Decreases Urinary Calcium Excretion and Serum 1,25-Dihydroxyvitamin D Concentrations in Idiopathic Hypercalciuria^*

Division of Nephrology and Internal Medicine and the Endocrinology Research Unit, Mayo Clinic and Mayo Foundation Rochester, Minnesota 55901

Address requests for reprints to: Dr. Christian J. Van Den Berg, Nephrology and Internal Medicine, Mayo Clinic, Rochester, New York 55901.

Orthophosphate treatment of patients with idiopathic hypercalciuria reduces the urinary excretion of calcium. To examine the role of altered vitamin D metabolism in reducing the renal excretion of calcium, we studied 11 patients with idiopathic hypercalciuria before and after 2 weeks of treatment with oral neutral orthophosphate (2 g phosphorus/day). Variables measured were urine calcium and phosphorus and serum calcium, phosphorus, immunoreactive parathyroid hormone, and 1,25-dihydroxyvitamin D [1,25-(OH)₂D]. Oral phosphate treatment significantly decreased urine calcium excretion [mean change (), –123 mg/24 h], increased urine phosphorus (mean A, +1039 mg/24 h), and decreased serum levels of 1,25-(OH)2D (mean A, –22 pg/ml). Pretreatment levels of 1,25-(OH)₂D were high when compared with levels in age-matched controls, whether assessed as the arithmetic mean (57 us. 33 pg/ml; P < 0.025), the logarithmically normalized (42 us. 27 pg/ml), or the median value (45 us. 24 pg/ml). Phosphate treatment decreased serum levels of 1,25-(OH)₂D to a mean of 35 pg/ml (logarithmically normalized mean, 22 pg/ml; median, 21 pg/ml), values not significantly different from those of normal controls. Serum calcium and phosphorus concentrations were not changed by treatment. Serum immunoreactive parathyroid hormone values increased minimally within the normal range (mean , +2 /µleq/ ml; P < 0.025). We conclude that the effect of oral phosphate therapy in decreasing urinary calcium excretion may involve the reduced synthesis of 1,25-(OH)₂D, independent of altered parathyroid function. (JClin Endocrinol Metab 51: 998, 1980)

^* This work was supported in part by Research Grants AM-20605, AM-19607, RR-585, and AM-25409 from the NIH, USPHS; the R. K. Mellon Foundation; the Minnesota Arthritis Foundation; and the Mayo Foundation.

Received February 19, 1980.

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