Magnesium (Mg) is a major intracellular cation, second only to potassium in abundance. In cells, Mg
is involved as a catalyst or activator in many enzymatic reactions; it is needed for all reactions
that utilize ATP, since a Mg-ATP complex is the immediate substrate in these. The majority of
the body's Mg is present in bone (50%) and skeletal muscle and soft tissue, while only roughly 1% is present in the
blood; thus, the level measured in serum or plasma is a poor indicator of total body stores.
Of the
Mg in blood, about 20-30% circulates bound to serum proteins (mainly albumin), while the
remainder is either free (60%) or bound to phosphates, citrates, and other compounds. The colorimetric
method used on the Hitachi here at Cornell measures total Mg. With ion-specific electrodes,
selective measurement of ionized Mg is possible.
Magnesium homeostasis is determined largely by the balance between intestinal absorption and
renal excretion. Overall, very little is known about the factors that control magnesium homestasis; indeed magnesium is referred to as the "forgotten" element. The kidneys play a pivotal role in controlling serum Mg levels by modulating
tubular reabsorption. 70-80% of Mg is filtered through the glomerulus. Of this, 20% is absorbed in the PCT, 70% in the thick ascending limb of the loop of Henle and 10% in the distal tubules. The control of reabsorption is complex; factors involved include dietary
content, several hormones (PTH, PTH-related protein, calcitonin, ADH, aldosterone, thyroxine and others), and serum
levels of Mg and Ca. Magnesium is also secreted in saliva (ruminants especially), sweat (horses) and mammary secretions.
Hypermagnesemia
- Artifact: Spurious elevations in Mg can be seen in hemolyzed samples due to release of Mg from erythrocytes.
- Increased intake: Excessive supplementation (fluids, diet).
- Decreased excretion: Reduced GFR in chronic renal failure or urinary tract obstruction, hypocalcemia (? renal antagonism with Mg) and Addison's disease. Oliguric or anuric renal failure in dogs and cats consistently
increases Mg levels.
- Release from cells: Since Mg is stored in skeletal muscle and soft tissue, massive tissue necrosis could releae
Hypomagnesemia
Magnesium levels should be measured under the following situations:
Unexplained hypocalcemia (Mg inhibits PTH or stimulates uptake of calcium into bone), resistant hypokalemia (if Mg is not administered, the hypokalemia is refractory to K supplementation), myopathy, neuromyopathy and critically ill animals. Magnesium is often decreased in critical patients and is associated with outcome. Whether the hypomagnesemia is a cause of increased morbidity or a result of the illness is not yet known and the hypomagnesemia is, as yet, unexplained. Very low levels of Mg result in cardiac arrest, weakness and convulsions.
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- Decreased intake: Decreased intake due to anorexia or insufficiency of Mg in the diet can lead to
hypomagnesemia. Other causes include administration of magnesium-poor fluids or total parenteral nutrition in small animals.
- Hypomagnesemia in ruminants: Cattle fed on rich spring grass pastures or dry feed that is low in Mg develop grass or hypomagnesemic tetany. Furthermore, fertilization of pastures with calcium, nitrates, ammonia, sulphates and potassium result in decreased Mg uptake into pastures. This syndrome occurs rapidly in dairy cattle, especially if pregnant or lactating as they have increased Mg demands. Grass tetany is characterized by severe hypomagnesemia, hypocalcemia (due to PTH resistance and inhibition of PTH secretion) and low or normal phosphate. Clinical signs are often precipitated by stress, such as reduced food intake, sudden decrease in dietary Mg, cold weather, transport etc. Transport tetany and winter tetany (associated with poor quality feed with decreased feed intake) are similar syndromes. Milk tetany occurs in calves fed whole milk, especially veal calves. Magnesium decreases by 6 weeks of age due to decreased absorption with age.
- Translocation into cells: Mg can move intracellularly in response to insulin, hypothermia or sepsis in horses. This is a postulated reason for hypomagnesemia in septic horses.
- Excessive loss
- Gastrointestinal tract: Decreased absorption or loss can occur with gastrointestinal conditions resulting in malabsorption or diarrhea.
Saliva is also high in Mg in ruminants, therefore loss of saliva in this species may result in hypomagnesemia (e.g. rabies, choke).
- Renal loss: Duiresis of any cause (administration of intravenous fluids, chemical or osmotic, e.g. diabetes mellitus) can result in increased urinary losses of Mg). Other causes of renal loss are hyperthyroidism (thyroid hormone decreases magnesium via unknown mechanisms), primary
hypoparathyroidism (PTH stimulates renal resorption of Mg and Mg release from bone), and acidosis.
- Cutaneous losses: Sweating in endurance or competitive horses. Sweat contains high concentrations of KCl, Mg and calcium. Endurance horses that sweat excessively are predisposed to hypokalemia, metabolic alkalosis, hypomagnesemia and hypocalcemia.
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