Causes and Management of Hypomagnesemia

Primary Mechanisms of Magnesium Depletion

Decreased gastrointestinal absorption or increased renal/intestine losses are the most common origins of hypomagnesemia, with medication‑induced renal wasting especially prevalent among hospitalized patients. 1
Chronic diarrhea and steatorrhea cause direct intestinal magnesium loss, leading to depletion. 1
Short bowel syndrome and jejunostomy reduce absorptive surface area, resulting in significant magnesium loss in the intestinal effluent. 2
Loop diuretics (e.g., furosemide) and thiazide diuretics inhibit magnesium reabsorption in the loop of Henle and distal convoluted tubule, respectively, making them frequent medication‑related causes of renal magnesium wasting. 1

Alterations in thyroid hormone levels can precipitate hypomagnesemia. 1
Secondary hyperaldosteronism secondary to sodium/water depletion increases renal excretion of both magnesium and potassium. 2
Hypomagnesemia impairs parathyroid hormone (PTH) release, producing refractory hypocalcemia that resolves only after magnesium repletion. 2

Hyperaldosteronism from volume depletion should be corrected before initiating magnesium replacement in patients with substantial gastrointestinal losses. [2][3]
Patients with short bowel and jejunostomy are prone to severe, refractory hypomagnesemia and often require early escalation to parenteral magnesium therapy. 3
Serum magnesium < 1.3 mEq/L defines hypomagnesemia, yet intracellular magnesium depletion may exist even when serum levels are normal or only mildly reduced. [1][3]
A normal serum magnesium concentration does not exclude intracellular deficiency; magnesium supplementation should be started whenever serum magnesium is reduced. 3
In the setting of gastrointestinal fluid losses, aggressive rehydration to correct hyperaldosteronism is the most important initial step before magnesium replacement. 3