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Reference Range

neonate 0.6 – 1.0
infant – 16y 0.7 – 1.0
adult 0.7 – 1.0

(note 24 hr urine magnesium range is 2.4 – 6.5 mmol/24h)

Test Usage

Magnesium is the fourth most abundant cation in the body, behind sodium, potassium, and calcium. It is the second most prevalent intracellular cation after potassium. The normal body magnesium content is approximately 1000 mmol or 25 g, of which about half is in bone and the other half is intracellular in soft tissue and muscle. Less than 1% of the total body magnesium is present in blood. Magnesium is essential for the function of many important enzymes, including reactions involving ATP synthesis and DNA replication and transcription. Magnesium is also required for cellular energy metabolism, membrane stabilization, nerve conduction, calcium channel activity and ion transport. Magnesium deficiency results in a variety of metabolic abnormalities and clinical consequences.

GI absorption and renal excretion regulate total body magnesium levels. The average daily dietary intake is about 325 mg and intestinal absorption is inversely proportional to the amount ingested. Most magnesium is absorbed in the ileum and colon. Cereal, grains, nuts legumes, and chocolate are relatively rich in magnesium. Vegetables, fruits, meats and fish have intermediate amounts and dairy products are low in magnesium. The kidney is the major excretory organ for magnesium. Approximately 70% of plasma magnesium is filtered through the glomerular membrane. Only about 6% of filtered magnesium (120 mg) is excreted daily into the urine, because of reabsorption in the Loop of Henle. The major regulator of tubular reabsorption is the plasma magnesium concentration. Hypermagnesemia inhibits and hypomagnesemia stimulates renal transport.

Serum magnesium exists in three states: approximately 60% is ionized (free), 33% is protein bound, and 7% is complexed to phosphate, citrate, and other anions. Approximately 75% of the protein bound fraction is bound to albumin and 25% to globulins. Serum magnesium concentration does not correlate very well with tissue magnesium levels. Serum levels are useful for assessing acute changes in magnesium states, especially in patients with cardiac arrhythmias, acute onset of seizures, and diabetic ketoacidosis.

Hypomagnesemia is found in 12 to 20% of hospitalized patients and up to 65% of patients in intensive care units. The usual reason is loss of magnesium from the GI tract or the kidney. The causes of magnesium depletion can be remembered as the “D” factors:

  • Diarrhea: Lower GI secretions are rich in magnesium. Diarrhea, malabsorption, bowel resection, steatorrhea and acute pancreatitis are common causes of magnesium depletion.
  • Diuretics: Loop diuretics can rapidly induce magnesium wasting. Long term thiazide diuretics can also cause hypomagnesemia.
  • Diabetes: This is the most common cause probably due to glycosuria and osmotic diuresis.
  • Drugs: mostly nephrotoxic drugs such as aminoglycosides, amphotericin B, cyclosporine, cisplatin, foscarnet, pentamidine.
  • Delivery: Magnesium normally declines by 10% in pregnancy and further during labor. Severe depletion is associated with eclampsia.
  • Denuded Skin: Burns are associated with a general loss of electrolytes.
  • Dietary: Hypomagnesemia becomes evident after 7 days of dietary magnesium restriction. Clinical signs are observed after 42 days.
  • Drinking: Alcohol inhibits renal tubular reabsorption of magnesium. Thirty percent of alcoholics admitted to the hospital have low magnesium.
  • Hypocalcemia is common in patients with severe hypomagnesemia, usually appearing when the serum magnesium level is less than 1.0 mmol/L. PTH levels are usually low and rise rapidly following magnesium replacement. Hyokalemia also frequently accompanies hypomagnesemia. It does not respond to potassium replacement until the magnesium deficit is corrected.

Hypermagnesemia is rare and usually iatrogenic. The most common causes are IV magnesium and magnesium containing cathartics or antacids. Patient most at risk are the elderly and those with bowel disorders or renal insufficiency. Clinical manifestations include hypotension, bradycardia, respiratory depression, depressed mental status, and ECG abnormalities.

Turnaround time

1 day


Local test

Can be added on to an existing request up to 4 days following sample receipt

Specimen Labelling Procedure
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