Osteocalcin Response to Low Calcium Diet: A Helpful Tool for the Differential Therapy of Hypercalciuria

Abstract

The treatment of idiopathic hypercalciuria is controversial. Low-calcium diets can induce osteopenia¹, and thiazide diuretics have side effects such as disturbances of uric acid and glucose metabolism, hypokalemia, and hypotension. Calcium-load tests and the measurement of serum osteocalcin levels on a free diet are not reliable enough to indicate appropriate management with calcium-restricted diet or thiazide therapy, respectively². This study was initiated to investigate whether the osteocalcin response to a calciumrestricted diet, reflecting bone turnover, is a potential tool in the metabolic investigation of hypercalciuria. Osteocalcin is a vitamin K-dependent, non-collagenous protein synthesized by osteoblasts³. Its synthesis is probably regulated by parathyroid hormone and 1,25-dihydroxyvitamin D. Serum levels (T1/2, 4–5 min) are determined by the activity of osteoblasts and mineralization. The highest concentrations are observed in states with increased osteoblastic activity and decreased mineralization³.