2. Discussion
Magnesium is the second most common intracellular divalent cation which functions as an allosteric modulator of several enzymes and is also responsible for bridging structurally distinct molecules [1]. One of the important functions of magnesium is to balance calcium levels in the intracellular fluids which in turn effect the neuromuscular junctions and the cardiovascular and central nervous systems [2]. Normal total plasma magnesium concentration varies in a narrow range (1.7–2.4 mg/dL). The kidney plays a crucial role in maintaining magnesium homeostasis. In the kidney about 10 percent of filtered magnesium is absorbed in the proximal tubule and 50 to 70 percent of the filtered magnesium is passively reabsorbed in the cortical aspect of the thick ascending limb of Henle [3].
There are 3 main processes via which hypermagnesemia can occur. The mechanism of hypermagnesemia includes-decreased elimination (as in case of renal insufficiency), magnesium overdose (as an infusion in treatment of severe preeclampsia/eclampsia or oral administration for use as an antacid or laxative), increased absorption as in case of impaired motility (drug induced opiates, anticholinergics; mechanical bowel obstruction). In our patient all the three mechanisms implicated for hypermagnesemia were operational: he had decreased elimination as a consequence of acute kidney injury and ingestion of multiple oral doses of milk of magnesia and had increased magnesium absorption secondary to the mechanical bowel obstruction from the sigmoid volvulus.
Presentation of hypermagnesemia depends on serum magnesium concentration (Table 1).