|Values are valid only on day of printing.|
Assessing the cause of abnormal serum magnesium concentrations
Determining whether the body is receiving adequate nutrition
Magnesium, along with potassium, is a major intracellular cation. Magnesium is a cofactor of many enzyme systems. All adenosine triphosphate-dependent enzymatic reactions require magnesium as a cofactor. Approximately 70% of magnesium ions are stored in bone. The remainder is involved in intermediary metabolic processes; about 70% is present in free form, while the other 30% is bound to proteins (especially albumin), citrates, phosphate, and other complex formers. The serum magnesium level is kept constant within very narrow limits. Regulation takes place mainly via the kidneys, primarily in the ascending loop of Henle.
Conditions that interfere with glomerular filtration result in retention of magnesium and, hence, elevation of serum concentrations. Hypermagnesemia is found in acute and chronic renal failure, magnesium overload, and magnesium release from the intracellular space. Mild-to-moderate hypermagnesemia may prolong atrioventricular conduction time. Magnesium toxicity may result in central nervous system depression, cardiac arrest, and respiratory arrest.
Numerous studies have shown a correlation between magnesium deficiency and changes in calcium-, potassium-, and phosphate-homeostasis, which are associated with cardiac disorders such as ventricular arrhythmias that cannot be treated by conventional therapy, increased sensitivity to digoxin, coronary artery spasms, and sudden death. Additional concurrent symptoms include neuromuscular and neuropsychiatric disorders. Conditions associated with hypomagnesemia include chronic alcoholism, childhood malnutrition, lactation, malabsorption, acute pancreatitis, hypothyroidism, chronic glomerulonephritis, aldosteronism, and prolonged intravenous feeding.
0-15 years: not established
> or =16 years: 75-150 mg/specimen
With normal dietary intake of 200 to 500 mg of magnesium per day, urine excretion is typically 75 to 150 mg/24 hours. The remainder of the dietary intake passes through the gastrointestinal tract and is excreted in the feces.
Decreased renal function, such as in dehydration, diabetic acidosis, or Addison's disease, results in reduced output of magnesium.
Poor diet (alcoholism), malabsorption, and hypoparathyroidism result in low urine magnesium due to low uptake from the diet.
Chronic glomerulonephritis, aldosteronism, and drug therapy (cyclosporine, thiazide diuretics) enhance excretion, resulting in high output of magnesium.
Magnesium forms insoluble complexes with normal urine constituents that precipitate as soon as urine is passed. Sodium bicarbonate must not be used as a preservative. Acidification not required.
1. Fentona TR, Eliasziw M, Lyon SC, et al: Low 5-year stability of within-patient ion excretion and urine pH in fasting-morning-urine specimens. Nutr Res 2009;29:320-326
2. Mircetic RN, Dodig S, Raos M, et al: Magnesium concentration in plasma, leukocytes and urine of children with intermittent asthma. Clin Chim Acta 2001;312:197-203