Magnesium Transport in Normal and Uremic Patients

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Abstract
The kinetics of radiomagneslum exchange in normal and uremic subjects was studied by administering high specific activity Mg28 intravenously and utilizing conventional and analog and digital computer techniques of data analysis. In normal subjects, the extracellular Mg (0.35 meq/kg) exchanged with 2 tissue Mg 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 3rd tissue Mg 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 Mg28 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 Mg was increased to 0.79 meq/kg. The fractional coefficients for influx into the 2 bidirectionally exchangeable tissue Mg pools and the unidirec-tionally exchangeable tissue Mg pool were decreased by 60%. Therefore, despite hypermagnesemia, the sizes and flux rates of these pools were normal. Urinary excretion of Mg28 was reduced to 44% of normal and urine specific activities were 19-26% higher than those of plasma. These data suggest that 1 tissue Mg 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 Mg may not provide a true estimate of Mg exchangeability. The urinary data further suggest the presence of a Mg fraction with this characteristic in renal tubular cells. In hyper-magnesemic uremia, an excessive intracellular accumulation of Mg does not occur since the cellular structures involve in Mg transport have the ability to reduce the fractional rate of cellular influx of Mg upon exposure to an elevated extracellular concentration of Mg. Studies of experimental hypermagnesemia suggest that this is a physiologic response to hypermagnesemia which is not impaired in the uremic state.

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