You are in: eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders HypermagnesemiaArticle Last Updated: May 16, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 8
  Author: Mahendra Agraharkar, MD, MBBS, FACP, President, Space City Associates of Nephrology; Medical Director, Chronic Home Dialysis Unit, DaVita Reliant Dialysis Center and DaVita South Shore Dialysis Center Mahendra Agraharkar is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and National Kidney Foundation Coauthor(s): Biruh T Workeneh, MD, Fellow in Nephrology, Stanford University School of Medicine; Mark Fahlen, MD, Staff Physician, Gould Medical Group Editors: Anil Kumar Mandal, MD, Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; George R Aronoff, MD, Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine; Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine; Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System Author and Editor Disclosure Synonyms and related keywords: excess magnesium, magnesium toxicity, magnesium overdose, magnesium overload, magnesium excess, renal failure, kidney failure, lithium therapy, hypothyroidism, Addison disease, familial hypocalciuric hypercalcemia, milk-alkali syndrome, milk alkali syndrome INTRODUCTIONSection 2 of 8
  Hypermagnesemia is an uncommon clinical finding, and symptomatic hypermagnesemia is even less common. This disorder has a low incidence of occurrence, because the kidney is able to eliminate excess magnesium by rapidly reducing its tubular reabsorption to almost negligible amounts. In healthy adults, plasma magnesium ranges from 1.7-2.3 mg/dL. Approximately 30% of total plasma magnesium is protein-bound and approximately 70% is filterable through artificial membranes (15% complexed, 55% free Mg2+ ions). With a glomerular filtration rate (GFR) of approximately 150 L/d and an ultrafiltrable magnesium concentration of 14 mg/L, the filtered magnesium load is approximately 2,100 mg/d. Normally, only 3% of filtered magnesium appears in urine; thus, 97% is reabsorbed by the renal tubules. In contrast to sodium and calcium, only approximately 25-30% of filtered magnesium is reabsorbed in the proximal tubule. Approximately 60-65% of filtered magnesium is reabsorbed in the thick ascending loop of Henle and 5% is reabsorbed in the distal nephron. Relatively little is known about cellular magnesium transport mechanisms. The most common cause of hypermagnesemia is renal failure. Other causes include the following:
RENAL FAILURESection 3 of 8
Patients with end-stage renal disease often have mild hypermagnesemia, and the ingestion of magnesium-containing medications (eg, antacids, cathartics) can exacerbate the condition. In patients undergoing regular dialysis, the serum magnesium level directly relates to the dialysate-magnesium concentration. In patients with acute renal failure, hypermagnesemia usually presents during the oliguric phase; the serum magnesium level returns to normal during the diuretic phase. If a patient receives exogenous magnesium during the oliguric phase, severe hypermagnesemia can result, especially if the patient is acidotic. OTHER CAUSESSection 4 of 8
People often take magnesium-containing medications (eg, antacids, laxatives, rectal enemas). Hypermagnesemia can develop after treatment of drug overdoses with magnesium-containing cathartics, and it also occurs in patients taking magnesium-containing medications for therapeutic purposes; however, most of these patients have normal renal function. If the patient does not ingest a large amount of magnesium but has a gastrointestinal disorder (eg, gastritis, colitis, gastric dilation), absorption may increase. In any case, monitoring serum magnesium levels in patients taking magnesium-containing medications is prudent. In the treatment of eclampsia, hypermagnesemia is induced deliberately and sometimes can be symptomatic. Occasionally, hypermagnesemia also can occur in the unborn infant. Maternal magnesium therapy can cause neurobehavioral disorders in the unborn child. Severe hypermagnesemia was described in patients who nearly drowned in the Dead Sea in Jordan, where magnesium levels average 400 mg/dL. Lithium therapy causes hypermagnesemia by supposedly decreasing urinary excretion, although the mechanism for this is not completely clear. Familial hypocalciuric hypercalcemia may cause modest elevations in serum magnesium. This autosomal dominant disorder is characterized by very low excretion of calcium and magnesium, and the increase in magnesium reabsorption appears to occur from an abnormal sensitivity of the loop of Henle to magnesium ions. Hypothyroidism, adrenal insufficiency, and milk alkali syndrome occasionally produce mild elevations of serum magnesium. EFFECTS OF HYPERMAGNESEMIASection 5 of 8
Symptoms of hypermagnesemia usually are not apparent unless the serum magnesium level is greater than 2 mmol/L. Concomitant hypocalcemia, hyperkalemia, or uremia exaggerate the symptoms of hypermagnesemia at any given level. Neuromuscular symptoms These are the most common presenting problems. Hypermagnesemia causes blockage of neuromuscular transmission by preventing presynaptic acetylcholine release and by competitively inhibiting calcium influx into the presynaptic nerve channels via the voltage-dependent calcium channel. One of the earliest symptoms of hypermagnesemia is deep-tendon reflex reduction. Facial paresthesias also may occur at moderate serum levels. Muscle weakness is a more severe manifestation, occurring at levels greater than 5 mmol/L. This manifestation can proceed to flaccid paralysis, then to depressed respiration, and, eventually, to apnea. Conduction system symptoms Hypermagnesemia depresses the conduction system of the heart and sympathetic ganglia. A moderate increase in serum magnesium can lead to a mild decrease in blood pressure, and a greater concentration may cause severe symptomatic hypotension. Magnesium also is cardiotoxic and, in high concentrations, can cause bradycardia. Occasionally, complete heart block and cardiac arrest may occur at levels greater than 7 mmol/L. Hypocalcemia Apparently, this occurs because the secretion of parathyroid hormone (PTH) decreases or because end-organ resistance to PTH occurs. Paralytic ileus develops from smooth-muscle paralysis, and mothers being treated with magnesium for preterm labor suppression are at risk. Hypermagnesemia may interfere with blood clotting through interference with platelet adhesiveness, thrombin generation time, and clotting time. Nonspecific symptoms These symptoms include nausea, vomiting, and cutaneous flushing. MEDICATIONSection 6 of 8
Prevention of hypermagnesemia is usually possible. Anticipate hypermagnesemia in patients who are receiving magnesium treatment, especially in those with reduced renal function. Initially, withdraw magnesium therapy, which often is enough in patients with mild-to-moderate hypermagnesemia. In patients with symptomatic hypermagnesemia that is causing cardiac effects or respiratory distress, antagonize the effects by infusing calcium gluconate. Calcium antagonizes the toxic effect of magnesium, and these ions electrically oppose each other at their sites of action. This treatment usually leads to prompt symptomatic improvement.
Drug Category: DiureticsAgents that promote magnesium excretion are effective.
Drug Category: Calcium saltsCalcium may moderate nerve and muscle performance in hypermagnesemia.
Drug Category: Antidiabetic agentsAgents that shift magnesium ions into cells are helpful.
ACKNOWLEDGMENTSSection 7 of 8
The primary author would like to acknowledge the clerical contributions of his secretary, Irene Montag. Her contributions are greatly appreciated. REFERENCESSection 8 of 8
Article Last Updated: May 16, 2006 |
