The production of secondary potassium depletion, sodium retention, nephrocalcinosis and hypercalcaemia by magnesium deficiency

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Abstract
The effects of dietary-Mg deficiency were studied in rats (mean initial weight 100 g). The animals grew little or lost weight and after 12 days developed peripheral vasodilatation and edema which lasted for a further 7-10 days. There was a progressive fall in Mg content in skeletal muscle to 78% of the control value after 64 days, described by the equation: muscle Mg (mg/kg of dry fat-free solids) = 102.6-0.353 (days on deficient diet). The K content of skeletal muscle fell to 80% of the initial content after 64 days, was closely correlated with muscle Mg (r = 0.93), and was described by the equation: muscle K = 73 + 3.55 (muscle Mg). The mean contents of muscle Na and Cl increased in the deficient group by 51 and 35 meq/kg from the control values of 92 and 60 meq/kg respectively. Assuming all muscle Cl to be extracellular, intracellular Na in muscle was calculated and found not to differ in the two groups. Mg and K con-centrations were unaltered in brain, liver and kidney. The Ca contents of muscle, brain and liver did not differ significantly in the two groups but there was a mean increase of 40 meq of Ca/kg in the kidneys of the deficient group from the control value of 12 meq/kg. Within 3 weeks there was a decline in Mg concentration in the femur to about half that of the control group. The plasma Mg concentration fell from the control value of 1.7 to about 0.4 meq/kg within 3 weeks and thereafter increased slightly. Plasma Na was slightly increased in the deficient group; the mean Ca concentration in the deficient and control groups was 6.4 and 5.3 meq/kg respectively. Nephrocalcinosis occurred only when hypercalcaemia was also present. The hypothesis is advanced that the K deficiency was due to impaired ion transport secondary to an effect of Mg deficiency on mitochondrial function.