Intravenous hyperalimentation or treatment of diabetic ketoacidosis without providing adequate magnesium, especially in a previously malnourished patient, can cause an abrupt fall in plasma magnesium levels. This is largely due to magnesium being "pulled" into cells with glucose or as new lean body mass is synthesized. Hypophosphatemia, which can also develop with IV hyperalimentation, can contribute to the hypomagnesemia.
Renal wasting of magnesium can be seen with loop diuretics, hypophosphatemia, ketoacidosis, aminoglycosides, and nephrotoxic chemotherapeutic agents.
The normal renal threshold for magnesium (1.5 to 2.0 meq/L) is significantly decreased by cisplatin, diuretics, hypercalcemia, growth hormone, thyroid hormone, and calcitonin. Cisplatin causes dose-dependent, cumulative, reversible renal tubular injury. Even when the glomerular filtration rate is not diminished by cisplatin, renal magnesium wasting along with a secondary hypocalcemia and hypokalemia may develop. Potassium wasting is thought to occur as a result of impaired ATP production when magnesium is low. This in turn impairs the function of the membrane Na+/K+ transport system and causes loss of the normal Na+/K+ gradient. The accompanying hypocalcemia may be due to (1) impaired PTH release by the parathyroid gland, (2) decreased peripheral sensitivity to PTH, or (3) abnormal blood-bone calcium balance independent of PTH.
PHYSIOLOGIC EFFECTS Magnesium is essential to a large number of vital enzymes, including membrane-bound ATPase. Consequently hypomagnesemia may result in a wide variety of neuromuscular, gastrointestinal, and cardiovascular changes ( Table .23r.lZ.).
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