Disorders of Magnesium Metabolism: Hypomagnesemia and Hypermagnesemia

Abstract

Magnesium ions are essential to all living cells. As the second most abundant intracellular cation, magnesium has a crucial role in fundamental metabolic processes such as DNA and protein synthesis, oxidative phosphorylation, enzyme function, ion channel regulation, and neuromuscular excitability. Hypomagnesemia is defined as a serum magnesium level less than 1.8 mg/dL (< 0.74 mmol/L). Hypomagnesemia may result from inadequate magnesium intake, increased gastrointestinal or renal losses, or redistribution from extracellular to intracellular space. Most patients with hypomagnesemia are asymptomatic and symptoms usually do not arise until the serum magnesium concentration falls below 1.2 mg/dL. The first step to determine the likely cause of the hypomagnesemia is to measure urinary magnesium and calcium. Asymptomatic patients should be treated with oral magnesium supplements. Parenteral magnesium should be reserved for symptomatic patients with severe magnesium deficiency (< 1.2 mg/dL). Hypermagnesemia is defined as a serum magnesium level >2.3 mg/dL (>0.96 mmol/L or >1.9 mEq/L) and much less common than hypomagnesemia. Hypermagnesemia occurs primarily in patients with acute or chronic kidney disease. Neuromuscular symptoms are the most common presentation of magnesium intoxication. Evaluation of hypermagnesemia includes the determination magnesium, potassium, phosphate, and calcium levels as well as renal biochemistry. Patients with normal renal function and mild asymptomatic hypermagnesemia require no treatment except the removal of all sources of exogenous magnesium. Treatment includes the administration of intravenous calcium gluconate or chloride

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