James T McCarthy Rajiv Kumar

Magnesium is an essential intracellular cation. Nearly 99% of the total body magnesium is located in bone or the intracellular space. Magnesium is a critical cation and cofactor in numerous intracellular processes. It is a cofactor for adenosine triphosphate; an important membrane stabilizing agent; required for the structural integrity of numerous intracellular proteins and nucleic acids; a substrate or cofactor for important enzymes such as adenosine triphosphatase, guanosine triphosphatase, phospholipase C, adenylate cyclase, and guanylate cyclase; a required cofactor for the activity of over 300 other enzymes; a regulator of ion channels; an important intracellular signaling molecule; and a modulator of oxidative phosphorylation. Finally, magnesium is intimately involved in nerve conduction, muscle contraction, potassium transport, and calcium channels. Because turnover of magnesium in bone is so low, the short-term body requirements are met by a balance of gastrointestinal absorption and renal excretion. Therefore, the kidney occupies a central role in magnesium balance. Factors that modulate and affect renal magnesium excretion can have profound effects on magnesium balance. In turn, magnesium balance affects numerous intracellular and systemic processes [1-12].

In the presence of normal renal function, magnesium retention and hypermagnesemia are relatively uncommon. Hypermagnesemia inhibits magnesium reabsorption in both the proximal tubule and the loop of Henle. This inhibition of reabsorption leads to an increase in magnesium excretion and prevents the development of dangerous levels of serum magnesium, even in the presence of above-normal intake. However, in familial hypocalciuric hypercalcemia, there appears to be an abnormality of the thick ascending limb of the loop of Henle that prevents excretion of calcium. This abnormality may also extend to Mg. In familial hypocalciuric hypercalcemia, mild hypermagnesemia does not increase the renal excretion of magnesium. A similar abnormality may be caused by lithium [1,2,6,10]. The renal excretion of magnesium also is below normal in states of hypomagnesemia, decreased dietary magnesium, dehydration and volume depletion, hypocalcemia, hypothyroidism, and hyperparathyroidism [1,2,6,10].

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