Magnesium Depletion

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CAUSES OF MAGNESIUM (Mg) DEPLETION

Poor Mg intake

Other

Starvation

Lactation

Anorexia

Extensive burns

Protein calorie malnutrition

Exchange transfusions

No Mg in intravenous fluids

Renal losses

see Fig. 4-14

Increased gastrointestinal Mg losses

Nasogastric suction

Vomiting

Intestinal bypass for obesity

Short-bowel syndrome

Inflammatory bowel disease

Pancreatitis

Diarrhea

Laxative abuse

Villous adenoma

The causes of magnesium (Mg) depletion. Depletion of Mg can develop as a result of low intake or increased losses by way of the gastrointestinal tract, the kidneys, or other routes [1,2,8-13].

Renal magnesium (Mg) wasting Thiazides(?)

Volume expansion

• Osmotic diuresis

Glucose Mannitol Urea

• Diuretic phase acute renal failure*

• Post obstructive diuresis

• Hypercalcemia*

• Phosphate depletion*

Chronic renal disease*

• Renal transplant*

• Interstitial nephritis*

Renal magnesium (Mg) wasting Thiazides(?)

Tubular defects

Bartter's syndrome Gitelman's syndrome Renal tubular acidosis Medullary calcinosis

Drugs/toxins

Cis-platinum Amphotericin B Cyclosporine Pentamidine ? Aminoglycosides* Foscarnet (?ATN) Ticarcillin/carbenicillin ? Digoxin

Electrolyte imbalances

Hypercalcemia* Phosphate depletion* Metabolic acidosis Starvation Ketoacidosis Alcoholism

Hormonal changes

Hyperaldosteronism

Primary hyperparathyroidism Hyperthyroidism Uncontrolled diabetes

FIGURE 4-14

Renal magnesium (Mg) wasting. Mg is normally reabsorbed in the proximal tubule (PT), cortical thick ascending limb (cTAL), and distal convoluted tubule (DCT) (see Fig. 4-9). Volume expansion and osmotic diuretics inhibit PT reabsorption of Mg. Several renal diseases and electrolyte disturbances (asterisks) inhibit Mg reabsorption in both the PT and cTAL owing to damage to the epithelial cells and the intercellular tight junctions, plus disruption of the electrochemical forces that normally favor Mg reabsorption. Many drugs and toxins directly damage the cTAL. Thiazides have little direct effect on Mg reabsorption; however, the secondary hyperaldosteronism and hypercalcemia effect Mg reabsorption in CD and/or cTAL. Aminoglycosides accumulate in the PT, which affects sodium reabsorption, also leading to an increase in aldosterone. Aldosterone leads to volume expansion, decreasing Mg reabsorption. Parathyroid hormone has the direct effect of increasing Mg reabsorption in cTAL; however, hypercalcemia offsets this tendency. Thyroid hormone increases Mg loss. Diabetes mellitus increases Mg loss by way of both hyperglycemic osmotic diuresis and insulin abnormalities (deficiency and resistance), which decrease Mg reabsorption in the proximal convoluted tubule and cTAL, respectively. Cisplatin causes a Gitelman-like syndrome, which often can be permanent [1,2,8-12].

Cardiovascular

Muscular

Electrocardiographic results

Cramps

Prolonged P-R and Q-T intervals,

Weakness

U waves

Carpopedal spasm

Angina pectoris

Chvostek's sign

?Congestive heart failure

Trousseau's sign

Atrial and ventricular arrhythmias

Fasciculations

?Hypertension

Tremulous

Digoxin toxicity

Hyperactive reflexes

Atherogenesis

Myoclonus

Neuromuscular

Dysphagia

Central nervous system

Skeletal

Seizures

Osteoporosis

Obtundation

Osteomalacia

Depression

Psychosis

Coma

Ataxia

Nystagmus

Choreiform and athetoid movements

SIGNS AND SYMPTOMS OF HYPOMAGNESEMIA

FIGURE 4-15

Signs and symptoms of hypomagnesemia. Symptoms of hypomag-nesemia can develop when the serum magnesium (Mg) level falls below 1.2 mg/dL. Mg is a critical cation in nerves and muscles and is intimately involved with potassium and calcium. Therefore, neu-romuscular symptoms predominate and are similar to those seen in hypocalcemia and hypokalemia. Electrocardiographic changes of hypomagnesemia include an increased P-R interval, increased Q-T duration, and development of U waves. Mg deficiency increases the mortality of patients with acute myocardial infarction and congestive heart failure. Mg depletion hastens atherogenesis by increasing total cholesterol and triglyceride levels and by decreasing high-density lipoprotein cholesterol levels. Hypomagnesemia also increases hypertensive tendencies and impairs insulin release, which favor atherogenesis. Low levels of Mg impair parathyroid hormone (PTH) release, block PTH action on bone, and decrease the activity of renal 1-a-hydroxylase, which converts 25-hydroxy-vitamin D3 into 1,25-dihydroxy-vitamin D3, all of which contribute to hypocalcemia. Mg is an integral cofactor in cellular sodium-potas-sium-adenosine triphosphatase activity, and a deficiency of Mg impairs the intracellular transport of K and contributes to renal wasting of K, causing hypokalemia [6,8-12].

Magnesium deficiency

Insulin resistance

Altered synthesis of eicosanoids

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