Magnesium, the fourth most common cation in the body, has been the recent focus of much clinical and scholarly interest. Previously underappreciated, this ion is now established as a central electrolyte in a large number of cellular metabolic reactions, including DNA and protein synthesis, neurotransmission, and hormone-receptor binding. It is a component of GTPase and a cofactor for Na+/K+ –ATPase, adenylate cyclase, and phosphofructokinase. Magnesium also is necessary for the production of parathyroid hormone. Accordingly, magnesium deficiency has an effect on multiple body functions.
Magnesium is present in greatest concentration within the cell and is the second most abundant intracellular cation after potassium. The total body content of magnesium is 2000 mEq. The intracellular concentration of magnesium is 40 mEq/L, while the serum concentration is 1.5-2 mEq/L. Most of the body's magnesium is found in bone. Only 1% of the total body magnesium is extracellular. Of this amount, one half is ionized, and 25-30% is protein bound.
Magnesium, a component of chlorophyll, is absorbed in the small bowel by active and passive transport mechanisms. Absorption of dietary magnesium takes place mainly in the ileum. It is excreted in stool and urine, but regulation of serum magnesium is under renal control. Most renal reabsorption of magnesium occurs in the proximal tubule and the thick ascending limb of the loop of Henle. In hypomagnesemic patients, the kidney may excrete as little as 1 mEq/L of magnesium. Additionally, magnesium may be removed from bone stores in times of deficiency.
A: Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is....
Clinical effects of hypomagnesemia are greatest in the CNS, neuromuscular, GI, and cardiac systems.
Risk of incidence is as follows:
Incidence is equal in males and females.
Magnesium deficiency may contribute to many age-related diseases.
The primary clinical findings are neuromuscular irritability, CNS hyperexcitability, and cardiac arrhythmias. The severity of symptoms is not related directly to the magnesium level. The reference range for serum magnesium level is 1.8-3 mEq/L. Usually, patients become symptomatic at 1.8 mEq/L. However, the physical findings may not be present in all cases. In one study of patients who were severely depleted of magnesium, abnormal physical findings were present in only 2 of 21 patients.
The causes of hypomagnesemia are numerous. Most causes are related to renal and GI losses.
Be attentive to the ABCs. At this point, the diagnosis usually is not known; therefore, advanced cardiac life support (ACLS) protocol should be followed. Seizures should be treated with benzodiazepines.
Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Oral replacement is appropriate for mild symptoms, while IV replacement is indicated for severe clinical effects.
These agents are used to replace an existing magnesium deficit.
Clinical Context: Oral supplementation should be given when patient is mildly depleted of magnesium (ie, magnesium level >1 mEq/L and patient is asymptomatic).
Other oral supplements (eg, magnesium oxide, magnesium hydroxide) may be used.
Clinical Context: Supplementation via IV infusion should be given to patients with moderately severe to severe depletion.
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. Terms: 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. Terms: 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.