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Specialty Endocrinology

Hypermagnesemia is an electrolyte disturbance in which there is a high level of magnesium in the blood.[1] It is defined as a level greater than 1.1 mmol/L.[2] Symptoms include weakness, confusion, decreased breathing rate, and cardiac arrest.[2]

Hypermagnesemia can occur in kidney failure and those who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives).[3] It is usually concurrent with other electrolyte disturbances such as a low blood calcium and/or high blood potassium level. Specific electrocardiogram (ECG) changes may be present.[2]

Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis.[2]

Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium.

Signs and symptoms[edit]

Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart. Magnesium acts as a physiologic calcium blocker, which results in electrical conduction abnormalities within the heart.

Clinical consequences related to serum concentration:

Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L.[4] As per Lu and Nightingale,[5] serum Mg2+ concentrations associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:

Kidney failure[edit]

Results from a longitudinal study with end-stage renal disease suggest that hypermagnesemia may retard the development of arterial calcifications in end-stage renal disease.[6] Significantly lower values of carotid intima-media thickness and aortic pulse wave velocity values, which are surrogate markers for vascular calcification, were observed in chronic kidney disease patients with high serum magnesium levels (0.90–1.32 mmol/L or 2.18–3.21 mg/dL) indicating a lower arteriosclerotic burden associated with a lower risk of cardiovascular events and mortality.[7] Consequently, people with CKD with mildly elevated magnesium levels could have a survival advantage over those with lower magnesium levels.[8]


Magnesium status depends on three organs: uptake in the intestine, storage in the bone and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly intestine or kidney.[9]

Predisposing conditions[edit]


For a detailed description of magnesium homeostasis and metabolism see hypomagnesemia.


Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic.[2]


Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:

Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:


  1. ^ "hypermagnesemia" at Dorland's Medical Dictionary
  2. ^ a b c d e Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045. 
  3. ^ Romani, Andrea, M.P. (2013). "Chapter 3. Magnesium in Health and Disease". In Astrid Sigel; Helmut Sigel; Roland K. O. Sigel. Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences. 13. Springer. pp. 49–79. doi:10.1007/978-94-007-7500-8_3. 
  4. ^ Pritchard JA (1955). "The use of the magnesium ion in the management of eclamptogenic toxemias". Surg Gynecol Obstet. 100: 131–140. 
  5. ^ Lu JF, Nightingale CH (2000). "Magnesium sulfate in eclampsia and pre-eclampsia". Clin Pharmacokinet. 38: 305–314. doi:10.2165/00003088-200038040-00002. PMID 10803454. 
  6. ^ Meema HE, Oreopoulos DG, Rapoport A (1987). "Serum magnesium level and arterial calcification in end-stage renal disease". Kidney Int. 32: 388–394. doi:10.1038/ki.1987.222. PMID 3669498. 
  7. ^ Salem S, Bruck H, Bahlmann FH, et al. (2012). "Relationship between magnesium and clinical biomarkers on inhibition of vascular calcification". Am J Nephrol. 35: 31–39. doi:10.1159/000334742. PMID 22179063. 
  8. ^ Massy ZA, Drüeke TB (2012). "Magnesium and outcomes in patients with chronic kidney disease: focus on vascular calcification, atherosclerosis, and survival" (PDF). Clin Kidney J. 5 (Suppl 1): i52–i61. doi:10.1093/ndtplus/sfr167. 
  9. ^ Jahnen-Dechent W, Ketteler M (2012). "Magnesium basics" (PDF). Clin Kidney J. 5 (Suppl 1): i3–i14. doi:10.1093/ndtplus/sfr163. 

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