![]() 25Initial low serum magnesium concentrations were suggested to correlate with poor outcome after traumatic brain injury. 23,24Surgical ICU patients with severe head injury also seem to be at high risk for hypomagnesemia, potentially because of polyuria induced by cerebral injury. The incidence increases to as high as 65% for patients in an intensive care unit (ICU), where hypalbuminemia, total parenteral nutrition, and the use of magnesium-wasting medications are commonly present. Magnesium depletion has been demonstrated in 7–11% of hospitalized patients. 22However, perioperative volume expansion of the extravascular fluid may decrease passive magnesium transport, thereby decreasing plasma magnesium concentrations. 20Preoperative bowel preparation, intraoperative serum loss, and chelation of magnesium by transfusion of citrate-rich blood products as reported for liver transplantation have been proposed as contributing. 18–21During abdominal cancer surgery, serum magnesium concentrations have been shown to correlate with the extent of resection, but underlying mechanisms also may be factors. 15Hypomagnesemia also occurs perioperatively and is commonly found in patients undergoing cardiothoracic or major abdominal surgery or thyroidectomies. Low magnesium may aggravate insulin resistance and predispose diabetic patients to cardiovascular disease. 16,17Diabetes mellitus is strongly associated with hypomagnesemia, possibly because of increased urinary losses. Clinically significant magnesium deficiency (symptoms usually occur at plasma concentrations less than 0.5 mm) is commonly associated with diarrhea, vomiting, and laxative abuse the use of loop and thiazide diuretics, angiotensin-converting enzyme inhibitors, cisplatin, aminoglycosides, or other nephrotoxic drugs and several endocrine disorders, such as parathyroid disease, hyperaldosteronism, and chronic alcoholism. Hypomagnesemia is defined as a plasma magnesium concentration of less than 0.7 mm and results mainly from inadequate dietary intake and/or gastrointestinal and renal losses. Clinical Relevance of Magnesium Disturbances However, individuals are highly vulnerable to hypermagnesemia with loss of renal function. ![]() Urinary excretion of magnesium is normally 5 mmol/day if renal function is adequate but can be decreased to less than 0.5% (∼ 0.03 mmol/day) in the event of magnesium deprivation caused by extrarenal losses. 15The human body is not able to rapidly mobilize magnesium stores and exchange them with circulating magnesium to keep plasma concentrations within normal limits. Parathormone and vitamin D stimulate magnesium renal and intestinal reabsorption, respectively, whereas insulin may decrease renal excretion of magnesium and enhance its cellular uptake. 14Regulation of magnesium transport lacks a specific endocrine control, although several hormones have been suggested to alter magnesium homeostasis. 13Patients with mutation in the TRPM6 gene experience severe hypomagnesemia and secondary hypocalcemia. As demonstrated for the small intestine, an active transcellular transport involving TRPM6, a member of the transient receptor potential family of cation channels, localized along apical distal convoluted tubule membranes and at brush-border membranes of the duodenum, seems to play a role. Little is known about the mechanisms underlying magnesium reabsorption in the distal convoluted tubule.
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