Hypomagnesemia Workup

  • Author: Tibor Fulop, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Nov 3, 2011
 

Approach Considerations

The majority of patients with clinical manifestations of magnesium deficiency have hypomagnesemia. Measurement of serum magnesium is relatively easy, and it has become the method of choice to estimate magnesium content, although its use in evaluating total body stores is limited. Magnesium assessment can also be made via red cell, mononuclear cell, or skeletal muscle intracellular content; 24-hour urinary excretion; fractional excretion (FE) of magnesium; and intracellular free magnesium ion concentration with fluorescent dye or nuclear magnetic resonance spectroscopy.

Two caveats should be considered when serum magnesium is used to diagnose magnesium deficiency. First, although only free magnesium is biologically active, most methods of assessing the serum content measure total magnesium concentration. Because 30% of magnesium is bound to albumin and is therefore inactive, hypoalbuminemic states may lead to spuriously low magnesium values.

The second caveat is that the major physiologic role of magnesium occurs at an intracellular level. Excluding magnesium deposited in the bone, which is poorly mobilized, the extracellular fluid space contains only 2% of total body magnesium and may not always accurately reflect the intracellular magnesium status. A person may have normal serum levels of magnesium but be intracellularly depleted and exhibit signs of magnesium deficiency. Unfortunately, no quick, simple, and accurate test is available to measure intracellular magnesium.

A surrogate for direct intracellular magnesium is the measurement of magnesium retention after acute magnesium loading. This method is useful only when the clinical suggestion of magnesium deficiency is strong in the setting of normomagnesemia (eg, unexplained cardiovascular or neuromuscular abnormalities).

A magnesium deficiency is indicated if a patient has reduced excretion (< 80% over 24 h) of an infused magnesium load (2.4 mg/kg of lean body weight given over the initial 4 h). However, the utility of this test is uncertain. Patients with malnutrition, cirrhosis, diarrhea, or long-term diuretic use typically have a positive test, whether or not they have signs or symptoms referable to magnesium depletion. It seems prudent, therefore, to simply administer magnesium to these patients if they have unexplained hypocalcemia and/or hypokalemia.

Protein, potassium, phosphate, and calcium

Because extracellular magnesium is protein bound, the patient's protein status is an important consideration in interpreting magnesium levels.

Hypomagnesemia contributes to hypokalemia. This condition may be due to defective membrane ATPase or urinary losses of potassium. In addition, hypophosphatemia has been found in patients with hypomagnesemia.

Hypocalcemia is caused by magnesium depletion, but the reason is not known. Some studies link hypomagnesemia to decreased parathyroid hormone levels and end-organ resistance to parathyroid hormone. Alterations in vitamin D metabolism contribute to hypocalcemia.

Electrocardiography and cardiac monitor

Findings in hypomagnesemia are nonspecific. Findings include ST segment depression; tall, peaked T waves; flat T waves or depression in the precordium; U waves; loss of voltage; PR prolongation; and widened QRS.

Next

Excretion Analysis

If hypomagnesemia is confirmed, the diagnosis can usually be obtained from the history. If no cause is apparent, the distinction between gastrointestinal and renal losses can be made by measuring the 24-hour urinary magnesium excretion or the FE of magnesium on a random urine specimen. The latter can be calculated from the following formula:

FEMg = [(UMg x PCr) / (PMg x UCr x 0.7)] x 100

In the above equation, U and P refer to the urine and plasma concentrations of magnesium (Mg) and creatinine (Cr). The plasma magnesium concentration is multiplied by 0.7, since only about 70% of the circulating magnesium is free (not bound to albumin) and therefore capable of being filtered across the glomerulus. The normal renal response to magnesium depletion is to lower magnesium excretion to very low levels. Thus, daily excretion of more than 1 mmol or a calculated FE of magnesium above 3% in a subject with normal renal function indicates renal magnesium wasting.

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Contributor Information and Disclosures
Author

Tibor Fulop, MD  Associate Professor of Medicine, Medical Director, Outpatient Dialysis Services, Department of Medicine, Division of Nephrology, University of Mississippi Medical Center

Tibor Fulop, MD is a member of the following medical societies: American College of Physicians and American Society of Diagnostic and Interventional Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP, FASN  Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and National Kidney Foundation

Disclosure: South Shore DaVita Dialysis Center Ownership interest Other

Mark T Fahlen, MD  Inc

Mark T Fahlen, MD is a member of the following medical societies: American College of Physicians and Renal Physicians Association

Disclosure: Nothing to disclose.

Helbert Rondon-Berrios, MD  Nephrology Fellow, Renal-Electrolyte Division, University of Pittsburgh Medical Center

Helbert Rondon-Berrios, MD is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Renal Physicians Association

Disclosure: Nothing to disclose.

Chief Editor

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

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose.

Howard A Blumstein, MD, FAAEM Assistant Professor of Surgery, Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine

Howard A Blumstein, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Enrique Grisoni, MD Associate Professor, Department of Surgery, Division of Pediatric Surgery, University Hospital of Cleveland, Rainbow Babies and Children's Hospital

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gunjeet K Kala, MD Clinical Instructor, Division of Pediatric Nephrology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences, Women and Children's Hospital of Buffalo

Gunjeet K Kala, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Nephrology, and American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Stephen Kemp, MD, PhD Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Nona P Novello, MD Associate Chair, Department of Emergency Medicine, Franklin Square Hospital

Nona P Novello, MD is a member of the following medical societies: American College of Emergency Physicians and Phi Beta Kappa

Disclosure: Nothing to disclose.

Karl S Roth, MD Professor and Chair, Department of Pediatrics, Creighton University School of Medicine

Karl S Roth, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Nutrition, American Pediatric Society, American Society for Clinical Nutrition, American Society of Nephrology, Association of American Medical Colleges, Medical Society of Virginia, New York Academy of Sciences, Sigma Xi, Society for Pediatric Research, andSouthern Society for Pediatric Research

Disclosure: Nothing to disclose.

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

James H Sondheimer, MD, FACP Associate Professor of Medicine, Wayne State University School of Medicine; Medical Director of Hemodialysis, Harper University Hospital at Detroit Medical Center; Medical Director, DaVita Greenview Dialysis (Southfield)

James H Sondheimer, MD, FACP is a member of the following medical societies: American College of Physicians and American Society of Nephrology

Disclosure: Nothing to disclose.

James E Springate, MD Associate Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Attending Physician, Department of Pediatrics, Division of Pediatric Nephrology, Women and Children's Hospital of Buffalo

James E Springate, MD is a member of the following medical societies: American Academy of Pediatrics, American Physiological Society, American Society of Pediatric Nephrology, International Pediatric Transplant Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Genzyme Grant/research funds Other

Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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A: Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is a lumen-positive voltage gradient generated by the reabsorption of NaCl. Terms: FHHNC (familial hypomagnesemia with hypercalciuria and nephrocalcinosis); ADH (autosomal-dominant hypocalcemia); FHH/NSHPT (familial hypomagnesemia/neonatal severe hyperparathyroidism). B: Magnesium reabsorption in the distal convoluted tubule. Active transcellular transport is mediated by an apical entry through a magnesium channel and a basolateral exit, presumably via a Na+/Mg2+ exchange mechanism. Terms: HSH (hypomagnesemia with secondary hypocalcemia); GS (Gitelman syndrome); IDH (isolated dominant hypomagnesemia). Source: Konrad M, Schlingmann KP, Gudermann T: Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol 2004; 286: F599-F605.
 
 
 
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