Hypermagnesaemia is defined as a serum magnesium concentration > 1.1 mmol/L.
Hypermagnesaemia is an uncommon condition. It is usually only seen in the context of renal impairment and excess administration of magnesium. The normal range of serum magnesium is 0.7-1.1 mmol/L.
Hypermagnesaemia is defined as a serum concentration > 1.1 mmol/L, but clinical symptoms usually only develop when the level rises > 2.0 mmol/L.
Magnesium is principally absorbed from the intestines and excreted by the kidneys.
Magnesium is absorbed in the intestines and excreted by the kidney in urine. Bone is the main reservoir of magnesium in the body, but exchange with serum concentrations is not freely accessible.
The average daily intake of magnesium is 15 mmol, of which 5 mmol (one third) is absorbed and the rest is lost in the bowel. The principal site of absorption is the small bowel, but the colon can absorb a small amount.
The kidneys are the principal site of magnesium excretion. An estimated 80% of serum magnesium is filtered at the glomerulus. From here the principal site of reabsorption is the Loop of Henle in the thick ascending limb.
Reabsorption of magnesium is by passive diffusion due to a favourable electrical gradient generated by the Na-K-2Cl cotransporter. Therefore, loop diuretics, which affect sodium and chloride reabsorption in the loop of Henle can affect magnesium reabsorption. Other diuretics such as thiazides also increase magnesium urinary excretion.
Other factors that influence magnesium reabsorption in the nephron include:
There are no major hormones that regulate magnesium and interaction with the magnesium stores in bone is slow. Therefore, a negative magnesium balance (e.g. from inadequate intake) quickly leads to hypomagnesaemia.
As magnesium is reliant on urinary excretion for clearance, a positive magnesium balance (e.g. intravenous infusion) in the context of renal impairment can lead to hypermagnesaemia.
Hypermagnesaemia typically develops in the context of renal impairment or excess administration of magnesium.
Patients with end-stage renal disease typically have elevated magnesium levels (1.0-1.5 mmol/L) due to impaired renal excretion. The actual level of magnesium is reflective of oral magnesium intake in the diet.
Sharp elevations in magnesium can be seen with the exogenous administration of magnesium (commonly in magnesium-containing antacids or laxatives).
Magnesium may be given orally or intravenously. Alternatively, magnesium may be a major component of a drug (e.g. antacid or laxative).
These rarer causes typically feature only mild elevations in magnesium:
Hypermagnesaemia is typically asymptomatic unless serum concentration is > 2 mmol/L.
The diagnosis of hypermagnesaemia is based on a serum magnesium concentration >1.1 mmol/L.
Hypermagnesaemia is typically an incidental finding on blood tests. This may be seen in a patient presenting to hospital for another reason or on routine bloods. In most situations, the hypermagnesaemia is mild and the patient is asymptomatic.
Alternatively, plasma magnesium concentration may be checked for a specific clinical concern (e.g. significant ingestion of magnesium-containing medications or repeated administration of intravenous magnesium). This is particularly important in at risk patients (e.g. chronic kidney disease).
The majority of patients are asymptomatic and no specific management is required.
Hypermagnesaemia predominantly occurs in patients receiving exogenous administration of magnesium or in those with pre-existing renal disease. Therefore, management should centre on prevention. This means avoiding magnesium-containing medications (e.g. laxatives) in patients with CKD and monitoring patients receiving magnesium replacement.
The treatment of acute, symptomatic hypermagnesaemia depends on the severity of symptoms and degree of renal impairment. Patients with severe symptoms or severe renal impairment are likely to need therapy to decrease magnesium levels.
Usually leads to a rapid improvement in magnesium concentration.
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