INTRODUCTION: This represents a case of successful medical management of severe magnesium toxicity without renal replacement therapy.
CASE PRESENTATION: We present the case of a 37 year old female with mental incapacitation from prior strokes admitted to the urology service for management of her bilateral renal calculi. After undergoing lithotripsy, the patient was started on Renacidin® 10% infusion therapy thru nephrostomy tubes with the goal of chemolysis of remaining stone fragments. On day five of infusion therapy, the patient was found unresponsive and a code blue was called. An arterial blood gas drawn prior to intubation was consistent with hypercapnic respiratory failure. Labwork was notable for a magnesium of 17.8mg/dl, bicarbonate of 38mg/dl, and an ionized calcium of 0.78mmol/L. Of note, the patient had normal kidney function with a stable creatinine. The patient was transferred to the intensive care unit for further management.
DISCUSSION: Renacidin® contains a combination of citric acid and magnesium carbonate and is meant to promote stone dissolution by cationic transfer. In this case, distal occlusion within the ureter likely resulted in buildup and systemic absorption of the drug. Although this medication has a long history of use, there are few prior published reports of magnesium toxicity secondary to Renacidin® therapy. Upon transfer to the intensive care unit, the Renacidin® infusion was stopped and the nephrology service was consulted. Since the patient was maintaining good urine output and had normal kidney function, the decision was made to forgo dialysis. Normal saline at 250ml/hr and a continuous infusion of calcium chloride were started. The following morning, magnesium and ionized calcium levels were 5.9mg/dl and 1.13mmol/L, respectively. The patient was extubated the morning after and transferred back to the floor without any residual deficits from this event. Magnesium is a major intracellular cation involved in many cellular and neuromuscular processes (1). The kidney is the major organ for maintaining magnesium homeostasis. Approximately 80% of the magnesium that is not protein bound is filtered thru the glomerulus, with 15-20% of this is resorbed mostly in the ascending loop of henle. This resorption process is inversely related to flow and also affected by the electrical gradient across the tubule (1). The amount of magnesium resorbed will be less in situations where there is increased tubular flow or where the positive transluminal charge is lost. The use of aggressive hydration with normal saline maintained this tubular flow and created a negative transluminal gradient with the chloride. Additionally, it increased the glomerular filtration rate, which increased the amount of magnesium excreted. Lastly, calcium and magnesium are resorbed together if either cation is low in the plasma (2). In essence, a state of hypocalcemia will promote both calcium and magnesium resorption in the loop of henle. The aggressive repletion of calcium in this patient was another away of inhibiting magnesium resorption. These physiologic principles in the setting of normal renal function afforded the patient a chance to avoid the risks associated with dialysis and a relatively quick and safe recovery.
CONCLUSIONS: This is the first published case of magnesium toxicity with a level greater than 17mg/dl that was managed without renal replacement therapy. It illustrates effective medical management of magnesium toxicity using principles of renal physiology.
Reference #1 Topf JM, Murray PT. Hypomagnesemia and Hypermagnesemia. Reviews in Endocrine And Metabolic Disorders 2003;4:195-206.
Reference #2 Quamme GA. Effect of hypercalcemia on renal tubular handling of calcium and magnesium. Canadian Journal of Physiology and Pharmacology 1982; 60:1275.
DISCLOSURE: The following authors have nothing to disclose: Sandeep Konka, Ali Massoumi, Allen Roberts, Shakil Aslam, Eldrige Pineda
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