Magnesium (Mg)


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Subject: Magnesium (Mg)

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  • Mg is primarily an intracellular ion associated with GI absorption and renal excretion. At least 65–70% of Mg is in ionized state, and approximately 35% serum Mg is protein bound.

  • Normal range: 1.6–2.4 mg/dL.

  • Critical values: <1.0 and >4.9 mg/dL.


  • Diagnosis and monitoring of hypomagnesemia and hypermagnesemia, especially in renal failure or GI disorders

  • To monitor preeclampsia patients being treated with magnesium sulfate, although in most cases, monitoring clinical signs (respiratory rate and deep tendon reflexes) is adequate, and blood magnesium levels are not required


Increased In

  • Iatrogenic (is usual cause; most often with impaired renal function).

    • Diuretics (e.g., furosemide >80 mg/day, thiazides)

    • Antacids or enemas containing Mg

    • Laxative and cathartic abuse

    • Parenteral nutrition

    • Mg for eclampsia or premature labor

    • Lithium carbonate intoxication

  • Renal failure (when GFR approaches 30 mL/minutes); in chronic renal failure, hypermagnesemia is inversely related to residual renal function. Increase is rarely observed with normal renal function.

  • Dehydration with diabetic coma before treatment

  • Hypothyroidism

  • Addison disease and after adrenalectomy

  • Controlled DM in older patients

  • Accidental ingestion of large amount of sea water

Decreased In

  • Almost always GI or renal disturbance; chronic Mg deficiency produces hypocalcemia secondary to decreased production and effectiveness of PTH.

    • GI disease

      • Malabsorption (e.g., sprue, small bowel resection, biliary and intestinal fistulas, abdominal irradiation, celiac disease, and other causes of steatorrhea; familial Mg malabsorption)

      • Abnormal loss of GI fluids (chronic ulcerative colitis, Crohn disease, villous adenoma, carcinoma of the colon, laxative abuse, prolonged aspiration of GI tract contents, vomiting)

    • Renal disease: a level >2 mEq/day in urine during hypomagnesemia indicates excessive renal loss.

      • Chronic GN

      • Chronic pyelonephritis

      • Renal tubular acidosis

      • Diuretic phase of acute tubular necrosis

      • Postobstructive diuresis

      • Drug injury

  • Diuretics (e.g., mercurials, ammonium chloride, thiazides, furosemide)

  • Antibiotics (e.g., aminoglycosides, gentamicin, tobramycin, carbenicillin, ticarcillin, amphotericin B)

  • Digitalis (in 20% of patients taking Digitalis)

  • Antineoplastic (e.g., cisplatin)

  • Cyclosporine: tubular losses due to ions or nutrients

  • Hypercalcemia

  • Diuresis caused by glucose, urea, or mannitol

  • Phosphate depletion

  • Extracellular fluid volume expansion

  • Primary renal Mg wasting

  • Nutritional

    • Prolonged parenteral fluid administration without Mg (usually >3 weeks)

    • Acute and chronic alcoholism and alcoholic cirrhosis

    • Starvation with metabolic acidosis

    • Kwashiorkor, protein–calorie malnutrition

  • Endocrine

    • Hyperthyroidism

    • Aldosteronism (primary and secondary)

    • Hyperparathyroidism and other causes of hypercalcemia

    • Hypoparathyroidism

    • DM (in ≤39% of patients; caused by osmotic diuresis)

  • Metabolic

    • Excessive lactation

    • Third trimester of pregnancy

    • Insulin treatment of diabetic coma

  • Other

    • Toxemia of pregnancy or eclampsia

    • Lytic tumors of bone

    • Active Paget disease of bone; caused by increased uptake by bone

    • Acute pancreatitis

    • Transfusion of citrated blood

    • Severe burns

    • Sweating

    • Sepsis

    • Hypothermia

  • Mg deficiency frequently coexists with other electrolyte abnormalities; it may cause apparently unexplained hypocalcemia and hypokalemia and should always be measured in such cases. About 40% of patients have coexisting hypokalemia.

  • About 90% of patients with high or low serum Mg levels are not clinically recognized; therefore, routine inclusion of Mg with electrolyte measurements has been suggested.

  • Digitalis sensitivity and toxicity frequently occur with hypomagnesemia.

  • Ionized Mg is decreased in only approximately 70% of critically ill patients with decreased total Mg.

  • Because deficiency can exist with normal or borderline serum Mg levels, a 24-hour urine test may be indicated by frequent concomitant disorders (coexist with other electrolyte abnormalities).

  • A 24-hour urine level <25 mg suggests Mg deficiency (in the absence of conditions or agents that promote magnesium excretion). If caused by renal loss, urine Mg should be >3.65–6 mg/day.

  • If level is <2.4 mg/day, collect a 24-hour urine sample during IV administration of 72 mg of MgCl2. Some 60–80% of the load is excreted by patients with normal Mg stores; <50% excretion suggests nonrenal Mg depletion.


  • Serum magnesium levels may remain normal even when total body stores of magnesium are depleted up to 20%.

  • Phylate, fatty acids, and an excess of phosphate impair Mg absorption

  • Hemolysis yields elevated results because levels in erythrocytes are two to three times higher than in serum.

Suggested Reading

Lum  G. Clinical utility of magnesium measurement. Lab Med.  2004;35:106.