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Pediatric Hypermagnesemia

  • Author: Alicia Diaz-Thomas, MD, MPH; Chief Editor: Stephen Kemp, MD, PhD  more...
 
Updated: Dec 11, 2015
 

Background

Magnesium is the second most abundant intracellular cation and the fourth most abundant cation overall. Almost all enzymatic processes using phosphorus as an energy source require magnesium for activation.[1] Magnesium is involved in most biochemical reactions such as glycolysis and oxidative phosphorylation. Because magnesium is bound to adenosine triphosphate (ATP) inside the cell, shifts in intracellular magnesium concentration may help to regulate cellular bioenergetics.[2, 3, 4]

Extracellularly, magnesium ions block neurosynaptic transmission by interfering with the release of acetylcholine. Magnesium ions also may interfere with the release of catecholamines from the adrenal medulla. In fact, magnesium has been proposed as being an endogenous endocrine modulator of the catecholamine component of the physiologic stress response.

Approximately 60% of total body magnesium is located in the bone, and the remainder is in the soft tissues. In this soft tissue intracellular compartment, which comprises about 38% of total body magnesium, relatively higher concentrations are found in the skeletal muscle and the liver. Because less than 2% is present in the extracellular fluid (ECF) compartment, serum levels do not necessarily reflect the status of total body stores of magnesium.

The reference range of serum concentration of magnesium is 1.8-2.5 mEq/L. Approximately one third of this magnesium is protein-bound. Analogous to plasma calcium, the free (ie, unbound) fraction of magnesium is the active component. Unfortunately, ionized serum magnesium cannot accurately be assessed at this time.

Less than 40% of dietary magnesium is absorbed; absorption takes place throughout the small intestine (predominantly in the ileum) and in the colon. A minimum daily intake of magnesium of 0.3 mEq/kg of body weight has been suggested to prevent deficiency. However, infants and children tend to have higher daily requirements of magnesium.

Elimination is predominantly renal; the threshold for urinary excretion nears the reference range of serum concentration. Thus, when serum levels are greater than 2.5 mEq/L, magnesium excretion dramatically increases. Conversely, the kidney retains a strong capacity to resorb magnesium, and the main site for reabsorption is the thick ascending loop of Henle.

(A) Magnesium reabsorption in the thick ascending (A) Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is a lumen-positive voltage gradient generated by the reabsorption of NaCl. FHHNC = Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. ADH = autosomal dominant hypocalcemia. FHH/NSHPT = Familial hypomagnesemia/neonatal severe hyperparathyroidism. (B) Magnesium reabsorption in the distal convoluted tubule. Active transcellular transport is mediated by an apical entry through a magnesium channel and a basolateral exit, presumably via a Na+/Mg2+ exchange mechanism. HSH = Hypomagnesemia with secondary hypocalcemia. GS = Gitelman syndrome. IDH = Isolated dominant hypomagnesemia. Source: Konrad M, Schlingmann KP, Gudermann T: Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol 2004; 286: F599-F605.

Renal reabsorption is impaired by several factors such as volume expansion, ethanol ingestion, hypercalcemia, and diuretic administration (eg, osmotic, thiazide, loop). Of these 3 types of diuretics, loop diuretics have a greater effect on renal magnesium wasting because of their site of action.[5]

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Pathophysiology

Hypermagnesemia is defined as a serum concentration greater than 2.5 mEq/L. (The reference range of serum magnesium levels is 1.8-2.5 mEq/L.) Most cases of hypermagnesemia have been noted in patients with severe renal failure in whom magnesium intake has been excessive. This may result from iatrogenic administration of medications that contain magnesium. Fatal hypermagnesemia has resulted from the administration of enemas containing magnesium to patients with renal failure. In fact, hypermagnesemia is rarely observed in individuals with a glomerular filtration rate (GFR) that is within reference range. In patients with acute renal failure and hypermagnesemia, levels usually remain less than 4 mEq/L.

Rapid mobilization of magnesium from soft tissues may result in hypermagnesemia following trauma, shock, cardiac arrest, or burns.

Hypermagnesemia usually occurs in individuals with significant diabetic ketoacidosis and often turns into hypomagnesemia during treatment. Thus, the initial hypermagnesemia is likely a pseudo-elevation secondary to dehydration, and the resulting hypomagnesemia may reflect intracellular shifting following insulin administration.

Neonates with hypermagnesemia whose mothers have received intravenous magnesium sulfate for pregnancy-induced hypertension may present with respiratory impairment, generalized hypotonia, and GI hypomotility mimicking intestinal obstruction. Pregnancy in women who have congenital cardiac disease is associated with increased risk, but favorable outcomes occur in most cases.[6]

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Epidemiology

Frequency

United States

Although the occurrence of hypermagnesemia has not been precisely defined, the disorder tends to occur in certain patient populations, particularly in patients with preexisting renal insufficiency.

Age

Although no age predisposition to developing hypermagnesemia is noted per se, neonates whose mothers have been treated with magnesium sulfate for eclampsia may be born with significant elevations in serum magnesium concentration, which can range from 3-11 mEq/L.

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Contributor Information and Disclosures
Author

Alicia Diaz-Thomas, MD, MPH Assistant Professor of Pediatrics, University of Tennessee Health Science Center

Alicia Diaz-Thomas, MD, MPH is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society, Tennessee Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, American College of Endocrinology

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Phyllis W Speiser, MD Chief, Division of Pediatric Endocrinology, Steven and Alexandra Cohen Children's Medical Center of New York; Professor of Pediatrics, Hofstra-North Shore LIJ School of Medicine at Hofstra University

Phyllis W Speiser, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

Robert J Ferry Jr, MD Le Bonheur Chair of Excellence in Endocrinology, Professor and Chief, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Eli Lilly & Co Grant/research funds Investigator; MacroGenics, Inc Grant/research funds Investigator; Ipsen, SA (formerly Tercica, Inc) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Grant/research funds Investigator; Bristol-Myers-Squibb Grant/research funds Other; Amylin Other; Pfizer Grant/research funds Other; Takeda Grant/research funds Other

Enrique Grisoni, MD Associate Professor, University Hospital of Cleveland, Department of Surgery, Division of Pediatric Surgery, Rainbow Babies and Children's Hospital

Disclosure: Nothing to disclose.

Anastasios K Konstantakos, MD Clinical Associate Surgeon, Department of Cardiovascular Surgery, Billings Clinic

Disclosure: Nothing to disclose.

References
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(A) Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is a lumen-positive voltage gradient generated by the reabsorption of NaCl. FHHNC = Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. ADH = autosomal dominant hypocalcemia. FHH/NSHPT = Familial hypomagnesemia/neonatal severe hyperparathyroidism. (B) Magnesium reabsorption in the distal convoluted tubule. Active transcellular transport is mediated by an apical entry through a magnesium channel and a basolateral exit, presumably via a Na+/Mg2+ exchange mechanism. HSH = Hypomagnesemia with secondary hypocalcemia. GS = Gitelman syndrome. IDH = Isolated dominant hypomagnesemia. Source: Konrad M, Schlingmann KP, Gudermann T: Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol 2004; 286: F599-F605.
 
 
 
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