Hypermagnesemia in Renal Failure

Abstract

Observations were made in 5 patients with severe renal failure who developed marked hypermagnesemia following the administration of Mg. In 2, Mg was given parenterally to treat a presumed state of Mg depletion and in the others antacid or laxative medications represented the source of excess Mg intake. Other patients with renal insufficiency were made hypermagnesemic experimentally by the ingestion or infusion of Mg compounds. The manifestations in all of these patients were quite similar; they included nausea, vomiting, malaise, hypotension, drowsiness, difficulty in voiding and defecating, dysarthria, ataxia of gait, decreased reflexes and respirations, coma, electrocardiographic changes, carotid sinus sensitivity and cardiac arrest. An attempt was made to correlate these manifestations with the serum Mg level. Recommendations are proposed for treating conditions of Mg depletion and Mg excess in patients with renal failure. The following conclusions are drawn regarding etiology: Severe renal disease limits the capacity to excrete Mg. This limitation is roughly proportional to the impairment in glomerular filtration rate. Mg contained in laxative and antacid medications, previously considered "non-reactive" or "non-absorbable", may be absorbed to a significant degree. Patients with severe renal failure ingesting customary doses of standard preparations may sustain significant elevations of the serum Mg with manifestations of toxicity in as little as 3 days.