Clinical Information

Magnesium, along with potassium, is a major intracellular cation. Magnesium is a cofactor of many enzyme systems. All adenosine triphosphate-dependent enzymatic reactions require magnesium as a cofactor. Approximately 70% of magnesium ions are stored in bone. The remainder is involved in intermediary metabolic processes; about 70% is present in free form, while the other 30% is bound to proteins (especially albumin), citrates, phosphate, and other complex formers. The serum magnesium level is kept constant within very narrow limits.

Renal handling of magnesium is determined by the combination of filtration and reabsorption. Roughly 70% of the magnesium in plasma is filtered by the glomeruli; 20% to 30% of the filtered magnesium is reabsorbed in the proximal tubule, while less than 5% is reabsorbed in the distal tubule and collecting duct.(1)

Numerous causes of renal magnesium wasting have been identified including (but not limited to) congenital defects (including Barter and Gitelman syndrome), various endocrine disorders (including hyperaldosteronism and hyperparathyroidism), exposure to certain drugs (ie, diuretics, cis-platinum, aminoglycoside antibiotics, calcineurin inhibitors), and other miscellaneous causes (including chronic alcohol abuse). Gastrointestinal conditions associated with fat malabsorption and chronic diarrhea can cause fecal magnesium loss and hypomagnesemia.

High levels of plasma magnesium are typically only seen in patients with decreased renal function, after administration of a magnesium load large enough to exceed the kidneys’ ability to excrete it, or a combination of the two.(2)

Magnesium is an inhibitor of calcium crystal growth, and contributes to urinary calcium oxalate and calcium phosphate supersaturation. However, low urinary magnesium in isolation has not been identified as a common cause of kidney stones, nor has magnesium supplementation been proven as an effective therapy for stone prevention.