The most common cause of hypermagnesemia in patients with renal failure is the indiscriminate use of magnesium-containing antacids. Increasing magnesium levels progressively reduce neuromuscular irritability and deep tendon reflexes. Deep tendon reflexes are lost prior to hypotension, cardiac abnormalities, or paralysis. IV calcium can counter the neuromuscular paralysis induced by hypermagnesemia. The primary treatment is saline and furosemide-assisted diuresis (contraindication: renal failure). Magnesium and calcium are poorly dialyzed. Hypomagnesemia may be secondary to chronic diuretic therapy, alcoholism, malnutrition, and diarrhea. Physical findings are similar to those of hypocalcemia and are predominantly neuromuscular (hyperreflexia, tetany, weakness, paresthesias, and carpopedal spasm), CNS (ataxia, confusion, seizures, and coma), and cardiac (arrhythmias, heart failure, and hypotension). When treating hypokalemia-associated arrhythmias, hypomagnesemia should be considered as well. IV administration of calcium is indicated in cardiac arrest secondary to hyperkalemic states.