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Effect of Magnesium Deficiency on Serum and Urinary Ions in Rats: Studies with Ion-selective Electrodes^1,2,

Department of Biochemistry and Nutrition, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061

The pathogenesis of the kidney calcification which appears in the young rat fed a low magnesium diet has not yet been adequately explained. Serum and urine concentrations of total calcium, magnesium and inorganic phosphate have been studied in deficient rats but the results have been variable. Measurement of free as well as total ions in a manner which would not disturb the equilibrium between the free ions and bound forms of these minerals would seem to be useful in the clarification of these questions. Calcium and divalent cation-selective electrodes were employed for this purpose in young rats trained to consume their daily ration within a 3-hour period. The results revealed that a marked increase in the proportion of free urinary calcium accompanied a significant hypocalciuria within 48 hours of the first low magnesium meal. Since these changes were compensatory, the ion product of octocalcium phosphate [Ca²⁺]⁴ [H⁺] [PO₄^3–]³ remained essentially constant and in the metastable region where a nucleating agent is necessary to initiate precipitation. Serum free and total calcium were unaffected in this study but the proportion of free magnesium rose as the deficiency progressed suggesting the existence of a magnesium ligand in serum. These findings are discussed in relation to a proposed hypothesis for kidney stone genesis in this model.

KEY WORDS: • magnesium • calcium • calcium ion • soft tissue calcification • kidney stones

¹ Supported in part by Public Health Service Research Grant no. AM 10446 from the National Institute of Arthritis and Metabolic Diseases and by U. S. Army Grant no. DAHC19-68-G-0021 from the Office of the Surgeon General.

² Presented in part at the First International Symposium on Magnesium Deficiency in Human Pathology, Vittel, France, May 9–15, 1971. Based upon a thesis submitted by James E. Bloomer in partial fulfillment of the requirements for the Ph.D. degree in Biochemistry and Nutrition at the Virginia Polytechnic Institute and State University.

³ Present address: Kennedy Laboratory, University of Wisconsin, Madison, Wisc.