Magnesium is one of the most abundant cations in the body and is essential for a wide variety of metabolically important reactions. Serum magnesium concentration is regulated by the balance between intestinal absorption and renal excretion. Hypomagnesaemia is relatively common, with an estimated prevalence in the general population ranging from 2.5 to 15%. It may result from inadequate magnesium intake, increased gastrointestinal or renal loss or redistribution from extracellular to intracellular space. Drug-induced hypomagnesaemia, particularly related to proton-pump inhibitor (PPI) therapy, is being increasingly recognized. Although most patients with hypomagnesaemia are asymptomatic, manifestations may include neuromuscular, cardiovascular and metabolic features. Due to the kidney's ability to increase fractional excretion to nearly 100% when the renal magnesium threshold is exceeded, clinically significant hypermagnesaemia is uncommon, generally occurring only in the setting of renal insufficiency and excessive magnesium intake. Symptoms include hypotension, nausea, facial flushing, ileus and flaccid muscle paralysis. In most cases, simply withdrawing exogenous magnesium is sufficient to restore normal magnesium concentrations, although occasionally administration of intravenous calcium or even dialysis may be required.