In both children and adults, fractional intestinal magnesium absorption is inversely proportional to the amount of magnesium ingested (Kayne and Lee, 1993). In balance studies, under controlled dietary conditions in healthy older men, an average of 380 mg (15.8 mmol)/day of ingested magnesium resulted in net absorption of approximately 40 to 60 percent; true absorption ranged from 51 to 60 percent for various foodstuffs when subjects were on a constant diet (Schwartz et al, 1984). Net absorption has been estimated to be 15 to 36 percent at higher daily intakes (550 to 850 mg [22.9 to 35.4 mmol]) and with varying levels of dietary bran and oxalate (Schwartz et al., 1986). Magnesium is absorbed along the entire intestinal tract, but the sites of maximal magnesium absorption appear to be the distal jejunum and ileum (Kayne and Lee, 1993). Both an unsaturable passive and saturable active transport system for magnesium absorption may account for the higher fractional absorption at low dietary magnesium intakes (Fine et al., 1991a).
A principal factor that regulates intestinal magnesium transport has not been described. Vitamin D and its metabolites 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D) enhance intestinal magnesium absorption to a small extent (Hardwick et al., 1991; Krejs et al., 1983). Recently, a low magnesium diet in rats was shown to increase intestinal calbindin-D9k. Although these preliminary data suggest a role for this vitamin D-dependent, calcium-binding protein in intestinal magnesium absorption, the severe magnesium deficiency imposed may have resulted in renal damage (not described) (Hemmingsen et al., 1994).
The kidney is the principal organ involved in magnesium homeostasis (Quamme and Dirks, 1986). The renal handling of magnesium in humans is a filtration-reabsorption process; there is no tubular secretion of magnesium. Approximately 65 percent of filtered magnesium is reabsorbed in the loop of Henle and 20 to 30 percent in the proximal convoluted tubule (Quamme and Dirks, 1986). Magnesium reabsorption in the proximal convoluted tubule appears to be passive; it follows changes in salt and water reabsorption and is associated with the rate of fluid flow. In the loop of Henle, there appears to be an additional active transport system: a decrease in magnesium reabsorption in this segment is independent of sodium chloride transport in either hypermagnesemia or hypercalcemia (Quamme, 1989). In vivo studies in animals and humans, however, have demonstrated a tubular maximum for magnesium that proba-