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. 1978 Mar;61(3):573–581. doi: 10.1172/JCI108968

Effect of Phosphate Depletion on Magnesium Homeostasis in Rats

Wilhelm J Kreusser 1, Kiyoshi Kurokawa 1, Enrique Aznar 1, Ellen Sachtjen 1, Shaul G Massry 1
PMCID: PMC372569  PMID: 641138

Abstract

The effects of phosphate depletion on magnesium (Mg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell significantly (P < 0.01) from 10.1±0.27 (SE) to 5.0±0.54 mg/100 ml within 1 day and continued to fall gradually to a level of 1.2±0.21 mg/100 ml by the end of the 8th wk. A significant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46±2.7 to 126±24 μeq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300±24 μeq/24 h by the 3rd day and remained high ranging between 150-300 μeq/24 h, thereafter. The magnitude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2±0.02 to 0.79±0.10 meq/liter by the 1st day of the study and remained low throughout.

Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which became evident by the 3rd wk of phosphate depletion. Mg content of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral content because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 μeq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or weight of the animals.

Our results indicate that phosphate depletion is associated with (a) magnesuria due to a decrease in the net renal tubular reabsorption of Mg with the main source of the urinary losses being bone Mg; (b) hypomagnesemia secondary to the renal leak of Mg; (c) negative Mg balance; and (d) increase in the intestinal fractional absorption of Mg. The latter was not adequate to compensate for the urinary losses of Mg.

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Selected References

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