Magnesium transport in normal and uremic patients.

Abstract

The kinetics of radiomagnesium exchange in normal and uremic subjects was studied by administering high specific activity 28Mg intravenously and utilizing conventional and analog and digital computer techniques of data analysis. In normal subjects, the extracellular magnesium (0.35 mEq/kg) exchanged with 2 tissue magnesium pools having sizes of 2.05 and 0.27 mEq/kg and bidirectional flux rates of 0.13 and 0.55 mEq/kg/hr, respectively. A third tissue magnesium pool of indeterminate size with an influx rate of 0.029 mEq/kg/hr and a negligibly small fractional efflux rate was also present. Urinary excretion of 28Mg averaged 10.4% dose/72 hr in the normal subjects and their urine specific activities were maintained at levels which were 23–40% higher than those of the plasma. In uremic patients with hypermagnesemia, the extracellular magnesium was increased to 0.79 mEq/kg. The fractional coefficients for influx into the 2 bidirectionally exchangeable tissue magnesium pools and the unidirectionally exchangeable tissue magnesium pool were decreased by 60%. Therefore, despite hypermagnesemia, the sizes and flux rates of these pools were normal. Urinary excretion of 28Mg was reduced to 44% of normal and urine specific activities were 19–26% higher than those of plasma. These data suggest that one tissue magnesium pool, because of a finite influx rate but a negligibly small fractional efflux rate, is capable of maintaining a specific activity above that of the plasma, and conventionally calculated exchangeable body pools of magnesium may not provide a true estimate of magnesium exchangeability. The urinary data further suggest the presence of a magnesium fraction with this characteristic in renal tubular cells. In hypermagnesemic uremia, an excessive intracellular accumulation of magnesium does not occur since the cellular structures involved in magnesium transport have the ability to reduce the fractional rate of cellular influx of magnesium upon exposure to an elevated extracellular concentration of magnesium. Studies of experimental hypermagnesemia suggest that this is a physiologic response to hypermagnesemia which is not impaired in the uremic state.