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Sample

  1. This test is done on the serum (3 to 5 mL clotted blood) of the patient.
    1. Fasting sample is preferred.
    2. Collect blood in the metal-free container.
    3. Separate the red cells immediately.
  2. Hemolysis interferes with the test. This may give false high value.
  3. Magnesium is Stable in blood for 3 hours and in serum at 2 to 8 °C for 8 hours.
  4. Separate the serum as soon as possible (within 45 minutes).
  5. Collect the sample in a prone position, because an upright position may increase magnesium by 4%.

Precautions

  1. Avoid hemolysis because it gives false high value.
  2. There are drugs which give rise to low value are diuretics, insulin, and few antibiotics.
  3. There are a few drugs which give high values are antacids, calcium-containing medicines, laxatives, and thyroid medicines.
  4. Fasting sample is preferred.
  5. Avoid venous stasis.

Purpose of the test

  1. To evaluate the renal function.
  2. To evaluate the electrolytes.
  3. To evaluate magnesium metabolism to find deficiency or overload.

Pathophysiology

  1. The magnesium is the fourth most abundant cation in the body.
    1. Mg concentration in the cell is second to Potassium.
    2. Extracellular concentration is much lower.
      1. 30% Mg in plasma bound to albumin.
      2. 70% Mg exist as the ion Mg²+.
  2. Majority of the magnesium is intracellular.
  3. Magnesium is stored in:
    1. Bone 40 to 60%.
    2. Within the cells 30%.
    3. Muscles 20%.
    4. Serum 1% (RBC).
  4. Distribution of the magnesium in the body is as follows:
    1. Skeleton                   =55%
    2. Soft tissue                = 45%
    3. Extracellular fluid  = 1%
    4. Total weight in grams   =  25 G
  5. Magnesium In the serum:
    1. 55% is free.
    2. 33% Associated with the protein (mainly albumin).
    3. 15% Complex with PO4, citrate and other anions.
    1. Magnesium intracellular and extracellular shown in the following diagram.

   

  1. Magnesium absorption and the source are:
    1. Meat.
    2. Green vegetables.   
    3. It is absorbed in the upper intestine.
      1. 50% absorbed by the active transport or passive diffusion in jejunum and ileum. 
      2. Vitamin D is not needed for the absorption. 
      3. Majority of the Mg is not absorbed because of the formation of insoluble phosphates and soap in the gut.

  1. The average human being weighing 70 Kg will have 24 grams of magnesium.

  1. When the serum magnesium is low then it leads to increased neuromuscular excitability because magnesium competes and inhibit the entry of calcium into neurons.
  2. Functions of Magnesium:
    1. Magnesium cofactor for >300 enzymes in the body. 
    2. Mg is important for the neuromuscular excitability.
      1. It has an important role for the smooth muscles contraction and relaxation. 
      2. In cardiac patient low magnesium level increase the irritability of the cardiac muscles and may lead to arrhythmias.
    3. Mg had synergistic action along with sodium, calcium and potassium ions.
    4. Magnesium helps with the absorption of calcium from the intestine.
    5. Magnesium deficiency mobilizes calcium from the bones.
    6. Magnesium deficiency may lead to abnormal calcification in the aorta and kidneys.
    7. It is important for the clotting mechanism.
    8. It has an important role in:
      1. Oxidative phosphorylation.
      2. Glycolysis.
      3. Cell replication.
      4. Protein Biosynthesis.
      5. Nucleotide metabolism (nucleic acid synthesis).
      6. Contraction of the muscular tissue.
    9. It is important for the action of ATP (adenosine triphosphate). It is bound to ATP molecule.
      1. It takes parts in phosphorylation which is the main source of energy.
  3. The kidney is the organ which the balance of Mg.
    1. Kidney will conserve when the intake is low and excrete the excess when the intake is high. 
    2. In damaged kidney with decreased renal function, magnesium may be retained in the body and increase serum level of magnesium.
    3. Aldosterone promotes the excretion of the Mg++ together with K+ and the retention of Na+.
  4. Increased magnesium (Hypermagnesemia)  is always due to increased intake of:
    1. Antacids.
    2. Enemas.
    3. Parenteral therapy in patients with renal failure.
    4. Administration of Mg in a patient with renal failure.
  5. This raised serum magnesium leads to:
    1. Decreased neuromuscular transmission (depression of neuromuscular system).
    2. Decrease the cardiac conduction.
    3. Slow deep tendon reflexes.
    4. There is respiratory depression.
  6. Magnesium-containing antacid may increase the magnesium level.
  7. Signs and symptoms of increased magnesium are:
    1. Lethargy.
    2. Slurred speech.
    3. Nausea and vomiting.
    4. Muscles weakness.
    1. Deep tendon reflexes disappear at the level of between 5 to 9 mg/dL.
      1. Depressed respiration is seen at 10 to 12 mg/dL.
      2. Hypotension.
      3. Bradycardia.
      4. Cardiac arrest at a higher level.
      5. ECG shows typical changes of:
        1. Tall T wave.
        2. Widened QRS.
        3. Flattened P wave.
        4. Increased PR interval.

  1. Hypomagnesemia when there is abnormally low serum magnesium.
    1. Low magnesium is seen in:
      1. Hospitals.
      2. Intensive care units. 
      3. Alcohol abuse increases the loss of magnesium in the urine.
  2. Sign and symptom of Low magnesium:
    1. Low magnesium level may lead to:
      1. Neuromuscular irritability with tetany and seizures.
        1. This is because Mg inhibits the entry of calcium into neurons.
      2. Cardiac arrhythmias may be seen. This may be related to hypokalemia and intracellular potassium depletion which occurs secondary to magnesium deficiency.
      3. Tachycardia and hypotension.
      4. Increased reflexes.
      5. Muscle cramps.
      6. Nystagmus.
    2. ECG changes are difficult to document in low Mg. It is associated with other electrolyte imbalance like hypokalemia and hypocalcemia.

Normal values

Source 1

Age mg/dL
Newborn 1.5 to 2.2
5 month to 6 year 1.7 to 2.3
6 to 12 year 1.7 to 2.1
12 to 20 year 1.7 to 2.2
Adult  
60 to 90 year 1.6 to 2.4
>90 year 1.7 to 2.3
Higher in females during menses

Source 2

Increased magnesium (hypermagnesemia) >2.5 meq/L level is seen in:

  1. Oral intake of Mg in the presence of chronic renal failure.
  2. Renal failure and oliguria.
  3. Dehydration.
  4. Addison’s disease.
  5. Diabetes mellitus uncontrolled (rare).
  6. Antacids containing magnesium.
  7. Hypothyroidism.
  8. Multiple myelomas.
  9. The enema containing Mg.
  10. Treatment of Mg deficiency.

Complication of Hypermagnesemia may cause respiratory paralysis and cardiac arrest. 

Decreased Magnesium (Mg deficiency) <1.0 meq/L level is seen in:

  1. Malabsorption (Kwashiorkor).
  2. Malnutrition (a diet low in protein intake).
  3. Prolonged nasogastric suction.
  4. Extensive bowel resection.
  5. Acute and chronic diarrhea.
  6. Intestinal and biliary fistula.
  7. Neonatal primary hypomagnesemia.
  8. Cirrhosis.
  9. Hypoparathyroidism.
  10. Hyperaldosteronism.
  11. Alcoholism chronic.
  12. Chronic renal tubular disease.
    1. Chronic pyelonephritis.
    2. Interstitial nephritis.
    3. Glomerulonephritis.
    4. Renal tubular acidosis.
    5. Postrenal transplantation.
    6. Phosphate depletion.
  13. Hypercalcemia of any cause (Hyperparathyroidism).
  14. Hemodialysis.
  15. Chronic pancreatitis.
  16. Long Term I/V therapy,
  17. Diabetic acidosis.
  18. Idiopathic cause.
  19. Drugs:
    1. Diuretic therapy (furosemide).
    2. Cisplatin.
    3. Cyclosporin.
    4. Amphoterin B.
    5. Cardiac glycosides.
  20. Increased Excretion  by the kidney:
    1. Tubular disorder.
    2. Pyelonephritis.
    3. Glomerulonephritis.
  21. Excess lactation.
  22. pregnancy.

Complication of Hypomagnesemia leads to tetany, delirium, agitation, muscle weakness and ultimately cardiac arrhythmias.

There may be decreased Calcium, Phosphate and Potassium level. 

Critical values are:


Possible References Used

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