Updated: Nov 18, 2019
Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP, FAMIA; Chief Editor: Eric B Staros, MD 

Reference Range

Magnesium is one of the major intracellular cations. For normal neuromuscular activity, humans need normal concentration of extracellular calcium and magnesium. Intracellular magnesium is an important cofactor for various enzymes, transporters, and nucleic acids that are essential for normal cellular function, replication, and energy metabolism.[1]

Normal findings[2] :

  • Adult: 1.3-2.1 mEq/L or 0.65-1.05 mmol/L (SI units)
  • Child: 1.4-1.7 mEq/L
  • Newborn: 1.4-2 mEq/L

Possible critical values[2] :

  • < 0.5 mEq/L or >3 mEq/L


Conditions causing an increase in magnesium levels

See the list below:

  • Iatrogenic (often with renal failure)

  • Diuretic (80 mg/day of furosemide or thiazide)

  • Antacids or enema containing magnesium

  • Laxative abuse

  • Parenteral nutrition

  • Magnesium therapy for eclampsia or premature labor

  • Lithium intoxication[3]

  • Renal failure

  • Dehydration diabetic ketoacidosis prior to therapy

  • Hypothyroidism

  • Addison disease and after adrenalectomy

  • Accidental ingestion of large amount of seawater

Conditions causing a decrease in magnesium levels

See the list below:

  • Gastrointestinal disease - Malabsorption, abnormal loss of gastrointestinal fluids as in ulcerative colitis, Crohn disease, villous adenoma, carcinoma of colon, laxative abuse, vomiting, prolonged aspiration of gastrointestinal tract[3] (Primary infantile hypomagnesemia and hypomagnesemia with secondary hypocalcemia are 2 rare genetic disorders that result in hypomagnesemia poor absorption from the gut.[1] )

  • Renal disease - Chronic glomerulonephritis, chronic pyelonephritis, renal tubular acidosis, diuretic phase of acute tubular necrosis, most obstructive diureses, drug injury, Bartter syndrome, Gitelman syndrome[1]

  • Diuretics

  • Antibiotics (aminoglycosides, amphotericin B, ticarcillin, carbenicillin)

  • Digitalis

  • Antineoplastic: cisplatin, cyclosporine, cetuximab[1, 4, 5]

  • Hypercalcemia

  • Diuresis caused by glucose, urea, mannitol

  • Phosphate depletion

  • Primary renal magnesium wasting

  • Extracellular fluid volume expansion

  • Nutritional - Prolonged total parenteral nutrition without magnesium, acute and chronic alcoholism, alcoholic cirrhosis, and starvation with metabolic acidosis, kwashiorkor, protein calorie malnutrition (Dietary magnesium deficiency is less likely except in the setting of alcohol abuse.)

  • Endocrine - Hyperthyroidism, hyperaldosteronism, hyperthyroidism, hyperparathyroidism, diabetes mellitus

  • Metabolic - Treatment with insulin, excessive lactation, third trimester of pregnancy

  • Others - Acute pancreatitis, eclampsia, lytic tumors of the bone, active Paget disease of bone, transfusion of citrated blood, severe burn, sweating, hypothermia, sepsis[3]

  • Prolonged use of proton pump inhibitors - Magnesium deficiency is seen with an increase in the prolonged use (probably for more than a year)[6] of proton pump inhibitors due to impairment in the intestinal absorption of magnesium.[7, 8, 9]


Collection and Panels

See the list below:

  • Collection: Tiger-top or red-top tube[10]




Magnesium is one of the major intracellular cations. For normal neuromuscular activity, we need normal concentration of extracellular calcium and magnesium. Intracellular magnesium is an important cofactor for various enzymes, transporters, and nucleic acids that are essential for normal cellular function, replication, and energy metabolism.[1] Fifty percent of the 25 g (1000 mmol) of total body magnesium resides in bone, whereas almost all of extraskeletal magnesium is located inside the cells. Serum magnesium levels may not accurately reflect the level of total body magnesium because only 1% of body magnesium is found in the extracellular fluid.[1]

About 30-40% of dietary magnesium (140–360 mg/d) is absorbed, principally in the jejunum and ileum. Absorption is stimulated by 1,25(OH)2 D and may reach 70% during magnesium deficit. Magnesium excretion in urine usually matches net intestinal absorption (100 mg/d). Serum magnesium concentration is regulated by renal magnesium reabsorption. About 60% of magnesium is reabsorbed in the cortical thick ascending limb of loop of Henle (cTAL), whereas 20% of filtered magnesium is reabsorbed in the proximal tubule, and another 5–10% in the distal convoluted tubule.[1] Parathyroid hormone increases magnesium reabsorption in the cTAL, whereas hypercalcemia and hypermagnesemia inhibit magnesium reabsorption.[1]

Magnesium (Mg) deficiency correlates with a higher mortality and worse clinical outcome, particularly in critical care patients. Magnesium has been directly implicated in hypocalcemia, tetany, hypokalemia, and arrhythmias.[11] Magnesium may play a role in stroke, ischemic heart disease, and bronchial asthma.[11, 12] An increased incidence of urinary stone disease is found in patients with dietary magnesium deficiency. Magnesium is a part of struvite calculi. Experimentally, dietary magnesium deficit is associated with increased calcium oxalate stone formation and calcium oxalate crystalluria.[13] Hypomagnesemia is a common electrolyte abnormality in heart failure and critical care patients; early detection and appropriate therapy to inhibit arrhythmogenic potential of magnesium deficit in such patients is advisable.[11, 14]

Patients with hypomagnesemia require frequent monitoring and magnesium replacement since this is correlated with adverse pathophysiological consequences, whereas hypermagnesemia is only a prognostic marker in patients with congestive heart failure.[15]


See the list below:

  • Diagnosis and monitoring of hypermagnesemia and hypomagnesemia particularly in patients with renal failure or with gastrointestinal problems

  • Monitoring therapy of patients with pre-eclampsia who are on magnesium sulfate (although in most cases, monitoring of clinical signs particularly respiratory rate and deep tendon reflexes is sufficient and blood magnesium level is not essential)[3]


Magnesium deficiency may coexist with other electrolyte deficiencies; it may cause unexplained hypocalcemia and hypokalemia, and, therefore, it should always be measured in such conditions. Approximately 40% of the patients have coexisting hypokalemia.[3] About 90% of the patients with high or low serum magnesium level are not clinically recognized; therefore, routine inclusion of magnesium with an electrolyte panel has been suggested. Ionized magnesium is decreased in the approximately 70% of critically ill patients with decreased total magnesium.[3]

Digitalis sensitivity and toxicity frequently occurs with hypomagnesemia.

Because deficiency can exist with normal or borderline serum magnesium level, a 24-hour urine test may be indicated. A 24-hour urine level less than 25 mg suggests magnesium deficiency (in the absence of conditions or agents that promote magnesium excretion). If the magnesium deficit is caused by renal loss, urine magnesium should be more than 3.625 to 6 mg per day.[3] If the level is less than 2.4 mg per day, collect 24-hour urine sample during IV administration of 72 mg of magnesium chloride. Some 60-80% of the load is excreted by patients with normal magnesium stores; less than 50% excretion suggests nonrenal magnesium depletion.[3]

Hypermagnesemia causes vasodilation and neuromuscular blockade (when the serum magnesium level is more than 4.8 mg/dL or 2 mmol/L).[1] Vasopressors or hypotension refractory to volume expansion is an early sign of hypermagnesemia. Muscular weakness, paralysis, respiratory failure, and coma, with decreased tendon reflexes, will occur when serum magnesium is more than 9.6 mg/dL. Paralytic ileus, flushing of face, dilation of pupils, paradoxical bradycardia, heart block, and prolongation of PR, QRS, and QT intervals are other features of magnesium toxicity. Asystole occurs when serum magnesium reaches 10 mmol/L.[1]

Magnesium deficiency causes muscle weakness, ataxia, nystagmus, vertigo, tetany, tremor, seizures, apathy, depression, irritability, delirium, and psychosis. Symptoms of magnesium deficit may not appear until serum magnesium level is less than 1.2 mg/dL.[1] The severity of symptoms may not correlate with serum magnesium levels. Sinus tachycardia, other supraventricular tachycardias, and ventricular arrhythmias may occur (QT prolongation may lead to torsades). Prolonged PR or QT intervals, flattening or inversion, of T-wave and ST straightening may appear in EKG.[1]

Hypocalcemia (with hypocalciuria) and hypokalemia may be seen in patients with hypomagnesemia. These abnormalities may not be easily corrected until the correction of magnesium deficit is achieved. Concomitant vitamin D deficiency may cause hypocalcemia; however, hypomagnesemia impairs the synthesis of 1,25(OH)2 D and cellular resistance to PTH. When the serum magnesium is less than 1 mg/dL, parathyroid hormone secretion is impaired.

Oral magnesium salts (MgO, MACl2) are used to treat mild hypomagnesemia. A note of caution: oral magnesium may result in diarrhea. Severe hypomagnesemia should be treated with intravenous magnesium chloride or magnesium sulfate (MgSO4 may cause hypocalcemia due to binding of calcium with sulfate). Intramuscular route of MgSO4 should be discouraged as it does not provide enough magnesium and is painful.[1]


Serum magnesium level may remain normal in spite of decreased total body store of magnesium (decreased up to 20%). Magnesium absorption is impaired by phytate, fatty acids, and increased phosphate.[3] Hemolysis causes increased results, for levels in RBC are 2-3 times higher than the serum.[1]