Hypomagnesemia An Evidence-Based Approach to Clinical Cases

Hypomagnesemia is defined as a serum magnesium level lessthan 1.8 mg/dL ( 0.74 mmol/L). Hypomagnesemia may resultfrom inadequate magnesium intake, increased gastrointestinal orrenal losses, or redistribution from extracellular to intracellularspace. Increased renal magnesium loss can result from genetic oracquired renal disorders. Most patients with hypomagnesemia areasymptomatic and symptoms usually do not arise until the serummagnesium concentration falls below 1.2 mg/dL. One of the mostlife-threatening effects of hypomagnesemia is ventricular arrhythmia.The first step to determine the likely cause of the hypomagnesemia isto measure fractional excretion of magnesium and urinary calciumcreatinineratio. The renal response to magnesium deficiency dueto increased gastrointestinal loss is to lower fractional excretionof magnesium to less than 2%. A fractional excretion above 2% ina subject with normal kidney function indicates renal magnesiumwasting. Barter syndrome and loop diuretics which inhibit sodiumchloride transport in the ascending loop of Henle are associatedwith hypokalemia, metabolic alkalosis, renal magnesium wasting,hypomagnesemia, and hypercalciuria. Gitelman syndrome andthiazide diuretics which inhibit sodium chloride cotransporterin the distal convoluted tubule are associated with hypokalemia,metabolic alkalosis, renal magnesium wasting, hypomagnesemia, andhypocalciuria. Familial renal magnesium wasting is associated withhypercalciuria, nephrocalcinosis, and nephrolithiasis. Asymptomaticpatients should be treated with oral magnesium supplements.Parenteral magnesium should be reserved for symptomatic patientswith severe magnesium deficiency ( 1.2 mg/dL). Establishmentof adequate renal function is required before administering anymagnesium supplementation.