Hypomagnesemia Medication

Updated: Aug 23, 2018
  • Author: Tibor Fulop, MD, PhD, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Medication

Medication Summary

Treatment for hypomagnesemia depends on the degree of deficiency and the patient's clinical symptoms and signs. Therapy can be oral for patients with mild symptoms or intravenous for patients with severe symptoms or those unable to tolerate oral administration. Some patients with hypomagnesemia caused by renal magnesium wasting may benefit from certain diuretics that have magnesium-sparing properties, such as spironolactone and amiloride.

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Magnesium Salts

Class Summary

Magnesium can be administered either orally in an oxide or gluconate form or parenterally as a sulfate salt.

Magnesium oxide (Mag-Ox, MagGel 600, Uro-Mag)

This agent is used for the treatment of magnesium deficiencies or magnesium depletion from malnutrition, restricted diet, alcoholism, or magnesium-depleting drugs.

Magnesium gluconate (Magtrate, Mag-G, Magonate)

Five hundred milligrams of magnesium gluconate contain 27 mg of elemental magnesium.

Magnesium sulfate

One gram of magnesium sulfate contains 8.12 mEq of magnesium (98 mg of elemental magnesium).

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Potassium-Sparing Diuretics

Class Summary

These medications are used to avoid the loss of potassium in urine.

Amiloride

Amiloride is a potassium-sparing diuretic that also has some mild hypocalciuric activity. It reduces the magnesium loss caused by thiazides. Amiloride is a pyrazine-carbonyl-guanidine that is chemically unrelated to other known antikaliuretic or diuretic agents. It possesses weak (compared with thiazide diuretics) natriuretic, diuretic, antihypertensive, and hypocalciuric effects.

In some clinical studies, amiloride activity increased the effects of thiazide diuretics. Amiloride is not an aldosterone antagonist, and its effects are observed even in the absence of aldosterone.

Amiloride exerts its potassium-sparing effect through the inhibition of sodium reabsorption at the DCT, the cortical collecting tubule, and the collecting duct. This decreases the net negative potential of the tubular lumen and reduces the secretion, and subsequent excretion, of potassium and hydrogen.

Amiloride usually begins to act within 2 hours after an oral dose. Its effect on electrolyte excretion peaks after between 6-10 hours and lasts about 24 hours. Peak plasma levels are obtained in 3-4 hours, and the drug's plasma half-life ranges from 6-9 hours.

Amiloride is not metabolized by the liver; it is excreted unchanged by the kidneys. About 50% of a dose of amiloride is excreted in urine and 40% is excreted in stool, within 72 hours. The drug has little effect on the GFR or on renal blood flow. Because the liver does not metabolize amiloride HCl, drug accumulation is not anticipated in patients with hepatic dysfunction; however, accumulation can occur if hepatorenal syndrome develops.

Amiloride rarely should be used alone. Used as single agents, potassium-sparing diuretics, including amiloride, result in an increased risk of hyperkalemia (approximately 10% with amiloride). Amiloride should be used alone only when persistent hypokalemia has been documented and only with careful titration of the dose and close monitoring of serum electrolytes.

Spironolactone (Aldactone)

Spironolactone is a potassium-sparing diuretic that acts on the distal convoluted tubule of the kidney as an aldosterone antagonist.

Triamterene (Dyrenium)

Triamterene interferes with potassium/sodium exchange (active transport) in the distal tubule, cortical collecting tubule, and collecting duct by inhibiting sodium/potassium adenosine triphosphatase (ATPase). This agent decreases calcium and magnesium excretion.

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