Hypermagnesemia: Causes, symptoms, and treatment
Hypermagnesemia: Causes, symptoms, and treatment
Authors:
Alan S L Yu, MB, BChir
Aditi Gupta, MD
Section Editors:
Michael Emmett, MD
Richard H Sterns, MD
Deputy Editor:
Albert Q Lam, MD
Literature review current through: May 2023.
This topic last updated: May 19, 2022.

INTRODUCTION

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].

Hypermagnesemia is an uncommon problem in the absence of magnesium administration or kidney failure. When it occurs, the elevation in the plasma magnesium concentration is usually mild (<3 mEq/L, 3.6 mg/dL, or 1.5 mmol/L) and the patient is asymptomatic. However, clinical symptoms may be seen when the plasma magnesium concentration exceeds 4 mEq/L (4.8 mg/dL or 2 mmol/L).

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

CAUSES OF HYPERMAGNESEMIA

The efficiency of the renal response to a magnesium load is such that hypermagnesemia is primarily seen in three settings: when kidney function is impaired; when a large magnesium load is given, whether intravenously, orally, or as an enema; or when there is increased absorption from the intestinal tract due to constipation, colitis, gastritis, or gastric ulcer disease [3,4]. Hypermagnesemia itself increases the neuromuscular blocking actions of magnesium, further increasing gastrointestinal magnesium absorption and resultant hypermagnesemia [3].

Kidney impairment — Hypermagnesemia can be seen in 10 to 15 percent of hospitalized patients, usually in the setting of kidney failure. Plasma magnesium levels rise as kidney function declines since there is no magnesium regulatory system other than urinary excretion [5]. The typical patient with end-stage kidney disease (ESKD), 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 [6]. 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 [7]. As a result, these drugs are contraindicated in patients with renal impairment.

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