Hypomagnesemia is a common entity occurring in up to 12 percent of hospitalized patients . The incidence rises to as high as 60 to 65 percent in patients in an intensive care setting in which nutrition, diuretics, hypoalbuminemia, and aminoglycosides may play important roles [2-5]. The kidney can, in the presence of magnesium depletion, lower magnesium excretion to very low levels; the stimulus for this response is a fall in the plasma magnesium concentration. (See "Regulation of magnesium balance".)
There are two major mechanisms by which hypomagnesemia can be induced: gastrointestinal or renal losses (table 1). Regardless of the cause, hypomagnesemia begins to occur after a relatively small magnesium deficit because there is little rapid exchange of extracellular magnesium with the much larger bone and cell stores.
Hypomagnesemia is often associated with hypokalemia (due to urinary potassium wasting) and hypocalcemia (due both to lower parathyroid hormone secretion and end-organ resistance to its effect). (See "Clinical manifestations of magnesium depletion".)
The major causes of hypomagnesemia will be reviewed in this topic. The regulation of magnesium balance, the signs and symptoms of hypomagnesemia, and the evaluation and treatment of patients with hypomagnesemia are presented elsewhere. (See "Regulation of magnesium balance" and "Clinical manifestations of magnesium depletion" and "Evaluation and treatment of hypomagnesemia".)
Gastrointestinal secretions contain some magnesium, and potential losses are continuous and not regulated. Although the obligatory losses are not large, marked dietary deprivation can lead to progressive magnesium depletion.