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Unit Code 8595:
Magnesium, Urine

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Useful For

Assessing the cause of abnormal serum magnesium

 

Determining whether the body is receiving adequate nutrition

Clinical Information

Magnesium along with potassium is a major intracellular cation.

Magnesium is a cofactor of many enzyme systems. All adenosine

triphosphate (ATP)-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 via 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

(CNS) 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 that have been associated with

hypomagnesemia include chronic alcoholism, childhood malnutrition,

lactation, malabsorption, acute pancreatitis, hypothyroidism, chronic

glomerulonephritis, aldosteronism, and prolonged intravenous feeding.

 

Reference Values

75-150 mg/specimen

Specimens collected for other than a 24-hour time period are reported

in unit of mg/L, for which reference values are not established.

Interpretation

With normal dietary intake of 200 mg to 500 mg of magnesium per day,

Urine excretion is typically 75 mg/24 hours 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.

Cautions

Magnesium forms insoluble complexes with normal urine constituents

that precipitate as soon as urine is passed. Acidification not required.

Sodium bicarbonate must not be used as a preservative.

 

Gadolinium is known to interfere with most metals tests. If gadolinium-

containing contrast media has been administered a specimen can

not be collected for 48 hours.

Special Instructions and Forms

• Urine Preservatives 
• Metals Analysis - Collection and Transport 

Clinical Reference

Elin RJ:  Assessment of magnesium status. Clin Chem 1987;33:1965-1970

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