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Causes and treatment of hypermagnesemia

Alan S L Yu, MB, BChir
Aditi Gupta, MD
Section Editor
Stanley Goldfarb, MD
Deputy Editor
Albert Q Lam, MD


The kidney is crucial in maintaining the normal plasma magnesium concentration in the narrow range of 0.7 to 1.1 mmol/L. In contrast to most other filtered solutes, only 10 percent of filtered magnesium is absorbed in the proximal tubule; most (50 to 70 percent) of the filtered magnesium is passively reabsorbed in the cortical aspect of the thick ascending limb of Henle [1,2]. Magnesium reabsorption at this site is paracellular and voltage dependent, mediated by the tight junction proteins, claudin-16 and claudin-19. Loop reabsorption is appropriately diminished with magnesium loading, thereby allowing the excess magnesium to be excreted in the urine [1].

The causes and treatment of hypermagnesemia are reviewed in this topic. The symptoms of hypermagnesemia, the normal regulation of magnesium balance, and the different units used to measure the plasma magnesium concentration are discussed separately. (See "Symptoms of hypermagnesemia" and "Regulation of magnesium balance".)


The efficiency of the renal response to a magnesium load is such that hypermagnesemia is primarily seen in two settings: when renal function is impaired and/or when a large magnesium load is given, whether intravenously, orally, or as an enema.

Renal insufficiency — Hypermagnesemia can be seen in 10 to 15 percent of hospitalized patients, usually in the setting of renal failure. Plasma magnesium levels rise as renal function declines since there is no magnesium regulatory system other than urinary excretion. The typical patient with end-stage renal disease (ESRD), for example, has a plasma magnesium concentration of 2 to 3 meq/L (2.4 to 3.6 mg/dL or 1 to 1.5 mmol/L). In patients on dialysis, the plasma magnesium concentration is primarily determined by magnesium intake. This was shown in a cross-sectional study of patients on hemodialysis who completed a dietary questionnaire; the correlation between estimated dietary magnesium intake and the serum magnesium was 0.87 [3]. In addition, hypermagnesemia (defined as a serum magnesium greater than 1.5 mmol/L) occurred with magnesium intakes as low as 281 mg/day, which is considerably lower than the average intake in the general population. Severe and symptomatic hypermagnesemia can also be induced when exogenous magnesium is given as antacids or laxatives in usual therapeutic doses [4]. As a result, these drugs are contraindicated in patients with renal impairment.

Magnesium infusion — Parenteral magnesium is commonly used to decrease neuromuscular excitability in pregnant women with severe preeclampsia or eclampsia. The usual plasma concentration achieved is 5 to 7 meq/L (6 to 8.4 mg/dL or 2.5 to 3.5 mmol/L), but much higher levels can occur. There are few prospective studies of complications associated with this regimen, but maternal hypocalcemia (since hypermagnesemia can suppress the release of parathyroid hormone) and hyperkalemia have been described, as have neonatal hypocalcemia, hypotonia, osteopenia, and an increased rate of admissions to the neonatal intensive care unit [5-10]. (See "Symptoms of hypermagnesemia".)

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Literature review current through: Sep 2017. | This topic last updated: Apr 27, 2017.
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