The many causes of clinical magnesium deficiency can be placed into 2 categories: diminished intake of magnesium, and enhanced losses of magnesium, either through the gastrointestinal tract or through the kidneys. Examples of the first category include alcoholism, starvation, anorexia due to neoplastic disease and/or chemotherapy. Examples of the second category include severe diarrhoeal states, gastrointestinal fistulae, malabsorption, diuretic therapy and gentamicin therapy. Estimates of the prevalence of clinical hypomagnesaemia range from 6 to 11% in hospitalised patients. Serum predictors of associated clinical magnesium depletion include hypokalaemia (42%), hyponatraemia (23%), hypophosphataemia (22%) and hypocalcaemia (20%). Experimental and clinical observations strongly support the view that magnesium and potassium are closely linked at the cellular level. Magnesium has been demonstrated to be important in cell energetics (Mg++-activated ATPase), in maintenance of the integrity of cell membranes, retardation of cell loss of potassium, as well as enhancing repletion of cell potassium. While translation of these experimental observations into clinical terms encompasses a wide spectrum of illnesses, there is special relevance in considering the role of magnesium in repletion and maintenance of cell potassium in 2 clinical instances: (a) patients treated with digitalis and diuretics; and (b) hypertensive patients. In these types of patients not only potassium but also magnesium should be administered together to avoid the problem of cell potassium depletion and refractory potassium repletion associated with coexisting and uncorrected magnesium depletion.