Normally, plasma magnesium ranges from 1.7-2.3mg/dL. However, magnesium levels may be elevated in up to 10-15% of patients at the hospital, particularly in those with kidney disease, since the magnesium is usually filtered through the kidneys, with 97% of the amount filtered being reabsorbed (10-30% on the proximal tubule, 50-70% on the loop of Henle and 5% on the distal tubule).


Renal insufficiency (reduced excretion)
Magnesium infusion
Oral ingestion (laxatives, antiacids)
Magnesium enemas (absorption through large bowel)
Lithium therapy
Addison disease
Familial hypocalciuric hypercalcemia
Milk alkali syndrome
Diabetic ketoacidosis
Hypercatabolic states (tumor lysis syndrome)


Elevated levels of magnesium can affect mainly the neuromuscular (decreases impulse transmission on the neuromuscular junction) and cardiovascular systems (magnesium acts as a calcium channel blocker, leading to bradycardia and hypotension). A brief summary of the effects of magnesium elevation according to the magnesium concentration is below:

  • 4-6 meq/L (4.8-7.2 mg/dL or 2-3 mmol/L) – Nausea, flushing, headache, lethargy, drowsiness, and diminished deep tendon reflexes.
  • 6-10 meq/L (7.2-12 mg/dL or 3-5 mmol/L) – Somnolence, hypocalcemia, absent deep tendon reflexes, hypotension, bradycardia, and ECG changes (prolongation of P-R and Q-T intervals, increased QRS duration, heart block).
  • >10 meq/L (12 mg/dL or 5 mmol/L) – Muscle paralysis (flaccid quadriplegia), apnea and respiratory failure, complete heart block, and cardiac arrest. In most cases, respiratory failure precedes cardiac collapse.


In many situations it is possible to predict and avoid the establishment of hypermagnesemia. Patients receiving IV magnesium should be monitored daily, and patients with renal failure should not receive medications containing magnesium.

If the patient has normal kidney function and diuresis, stopping the cause (removing the magnesium source, e.g. stopping infusion or oral intake) may be enough to reduce the magnesium levels.

However, patients with moderate reduction of the eGFR (15-45mL/min/1.73 m2) or severe reduction of the eGFR (<15mL/min/1.73 m2) should receive, in addition to the cessation of magnesium, normal saline associated with a diuretic (furosemide).

Patients with severe and/or symptomatic hypermagnesemia and advanced CKD or AKI may need dialysis.

While waiting for dialisis, symptomatic patients should also receive calcium (100-200mg of elemental calcium, or 10-20mL of 10% calcium gluconate IV over 5-10 minutes) to reduce neuromuscular and cardiac effects of hypermagnesemia.


  1. Fulop T. Hypermagnesemia. Medscape. Updated: May 06, 2015.
  2. Rude RK. ASBMR Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. Chapter 70. Magnesium Depletion and Hypermagnesemia. Pg. 325-328.