Table 5.

Settings in which symptomatic hypomagnesaemia might occur

Decreased dietary intake:

Malnutrition

Parenteral infusions without magnesium

Gastrointestinal malabsorption and loss [6]:

Severe or prolonged chronic diarrhoea [6–8]

Increased renal loss [6]:

Congenital or acquired tubular defects (see de Baaij et al. [48] in this supplement)

Drug induced:

Loop diureticsa [7, 74]

Aminoglycosides [7, 8, 70, 75]

Amphotericin B [8, 76]

Cyclosporine [8, 77] and tacrolimus [78]

Cisplatin [8, 79]

Cetuximab [80]

Omeprazole [81]

Pentamidine [8, 82]

Foscarnet [83]

Endocrine causes:

Primary and secondary hyperaldosteronism [8, 84]

Hungry bone syndrome, e.g. after surgery of primary hyperparathyroidismb [7, 8]

Syndrome of inappropriate anti-diuretic hormone hypersecretion

Diabetes mellitus [6, 8]

Other causes:Stress

Chronic alcoholismc [7, 8]

Excessive lactation, heat, prolonged exercise [6]

Severe burns [6, 85]

Cardiopulmonary bypass surgery [86]

Iatrogenic [6]

^aLoop diuretics such as furosemide, torasemide, ethacrynic acid, bumethanide and piretanide cause an increased urinary excretion [74]. Thiazide diuretics, acting on the early distal tubule, might lead to magnesium loss only in the long run [87]. In contrast, potassium-sparing diuretics, such as triamterene and amiloride acting on the late distal tubule, contribute to magnesium conservation by the kidneys. Osmotic agents such as mannitol or glucose hamper tubular re-absorption and augment magnesium excretion [7, 52].

^bHypomagnesaemia—due to deposition of magnesium in the calcium- and magnesium-depleted bone—occurs in one third of the patients after surgical correction of primary hyperparathyroidism [7].

^cIt was observed that chronic alcohol consumption goes along with a significant increase of urinary magnesium excretion and a reduced muscle magnesium content. Thus, empiric use of magnesium replacement therapy was suggested as part of the therapeutic alcohol withdrawal syndrome regimen [7].