Hypomagnesemia - approach to the patient

Overview and Recommendations

Background

Hypomagnesemia is defined as serum magnesium concentration < 1.8 mg/dL (0.75 mmol/L).
The reference range varies between laboratories, and the lower limit of normal may be defined
as low as 1.5 mg/dL (0.62 mmol/L).
The reported prevalence of hypomagnesemia ranges from 2.5% to 15% in the general
population, but it is higher among critically ill patients.
Hypomagnesemia may be acquired or have a genetic cause.
Mechanisms involved in the development of hypomagnesemia include:
redistribution of magnesium from extracellular to intracellular compartment (for example,
treatment of diabetic ketoacidosis)
decreased intestinal absorption (for example, due to malnutrition)
increased urinary excretion (for example, from ingestion of drugs such as diuretics)

Evaluation

Most patients are asymptomatic until the serum magnesium concentration is < 1.2 mg/dL (0.5
mmol/L), but some patients remain asymptomatic even with severe hypomagnesemia.
Patients with hypomagnesemia may present with symptoms that overlap with that of other
biochemical abnormalities, such as hypokalemia and hypocalcemia.
Early presentation of hypomagnesemia may include nausea, vomiting, and weakness.
Worsening deficiency may lead to numbness, muscle tingling, or cramps.
Severe hypomagnesemia (serum magnesium < 1 mg/dL [0.4 mmol/L]) may lead to seizures,
drowsiness, confusion, or coma.
Obtain a complete medical history and history of medications and look for the use of drugs
known to cause hypomagnesemia.
Signs to look for during a physical exam include signs of vertical nystagmus, tetany, or
muscular fasciculations.
Tests to determine underlying etiology:

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 Urine studies to differentiate renal wasting from gastrointestinal losses:
Calculate fractional excretion of magnesium (FEMg) on spot urine.
24-hour urinary magnesium excretion may be performed if the complete 24-hour
collection of specimen can be collected (rarely performed).
Interpreting Urine Studies of Hypomagnesemia:
Result Indicates GI
Result Indicates Renal
Urine Test Losses +/- Reduced
Wasting
Intake
FEMg > 2% < 2%
24-hour urinary excretion High (> 24 mg [1 mmol]) Low (< 12 mg [0.5 mmol])
Abbreviations: FEMg, fractional excretion of magnesium; GI, gastrointestinal.
Consider performing an electrocardiogram in patients with unexplained arrhythmias.
Consider genetic testing if inherited hypomagnesemia is suspected (positive family
history, hypomagnesemia without other explanation or that is discovered in infancy).

Management

The mode of treatment (magnesium supplementation) depends on the severity of magnesium

deficiency:
For patients with severe or symptomatic hypomagnesemia, give IV magnesium sulfate
with a treatment goal of serum magnesium concentration > 1 mg/dL (0.411 mmol/L).
For patients with asymptomatic hypomagnesemia, consider oral magnesium
supplementation, preferably with sustained-release magnesium. The usual dose is 2-4
tablets (60-96 mg [2.5-3.5 mmol]) per day.
Treat concomitant hypokalemia and/or hypocalcemia, if present.
For patients who cannot discontinue diuretic therapy (patients with chronic renal magnesium
wasting or diuretic-induced hypomagnesemia), consider the addition of a potassium-sparing
diuretic such as amiloride or triamterene.

Related Summaries
Hypokalemia
Hypermagnesemia - approach to the patient
Gitelman syndrome
Bartter syndrome

General Information
Description

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 hypomagnesemia is defined as serum magnesium concentration < 1.8 mg/dL (0.75 mmol/L);
reference range varies between laboratories, and lower limit of normal may be defined as low as
< 1.5 mg/dL (0.62 mmol/L)((1, 2, 3), QJM 2016 Jul;109(7):453)
typically asymptomatic until serum magnesium concentration < 1.2 mg/dL (0.5 mmol/L)(1)

Incidence/Prevalence

reported prevalence in general population ranges from 2.5% to 15%(1)

higher prevalence in critically ill patients
reported prevalence 65% in intensive care patients(1)
in cohort of 65,974 adults (mean age 62 years) admitted to Mayo Clinic (Rochester,
Minnesota), hypomagnesemia (< 1.7 mg/dL [0.7 mol/L]) reported in 20% (Mayo Clin
Proc 2015 Aug;90(8):1001 full-text), editorial can be found in Mayo Clin Proc 2015
Aug;90(8):993
in cohort of 100 critically ill children (mean age 4.9 years) admitted to pediatric intensive
care unit in India, hypomagnesemia (≤ 1.7 mg/dL [0.7 mmol/L]) reported in 55% (J Trop
Pediatr 2003 Apr;49(2):99EBSCOhost Full Text)
in cohort of 106 patients (median age 24.5 years) with cystic fibrosis being assessed for
lung transplantation, hypomagnesemia (< 1.8 mg/dL [0.74 mmol/L]) reported in 57% (J
Cyst Fibros 2007 Sep;6(5):360 full-text)
in cohort of 61 persons with chronic alcohol use disorder, hypomagnesemia (< 1.6 mg/dL [0.65
mmol/L]) reported in 30% (N Engl J Med 1993 Dec 23;329(26):1927 full-text)
in cohort of 541 adolescents (mean age 16.2 years) with eating disorder being "refed" with
standard nutrition and high-energy liquid supplements at tertiary care children's hospital,
hypomagnesemia (≤ 1.7 mg/dL [0.7 mmol/L]) reported in 15.9% (Nutr Clin Pract 2012
Oct;27(5):689)

Differential Diagnosis
Causes

Redistribution of magnesium from extracellular to intracellular compartment

treatment of diabetic ketoacidosis (insulin)(1, 4)

refeeding syndrome(1)
hungry bone syndrome after parathyroidectomy(1, 2, 4)
correction of metabolic acidosis(1)
acute pancreatitis (1, 4)

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 ethanol withdrawal syndrome(4)

Decreased intestinal absorption of magnesium

poor diet alone not likely to cause hypomagnesemia, but may exacerbate it when occurs in
conjunction with other symptoms like diarrhea (Rev Endocr Metab Disord. 2003 May;4(2):195)
decreased intestinal absorption of magnesium due to inadequate intake may occur with(1, 2)
malnutrition
alcohol use disorder
anorexia nervosa
terminal cancer
total parenteral nutrition
decreased intestinal absorption of magnesium due to increased gastrointestinal loss may be
caused by(1, 2)
acute or chronic diarrhea
malabsorption and steatorrhea
small bowel bypass surgery
vomiting and nasogastric suction
gastrointestinal fistulas
laxative abuse
short bowel syndrome
proton pump inhibitors (PPI) (exact mechanism unknown but appears to reduce intestinal
absorption of magnesium)(1)
FDA warns of possible increased risk of hypomagnesemia with long-term proton pump
inhibitor (PPI) use
FDA recommends evaluating serum magnesium levels
prior to initiating long-term PPI therapy
in patients concurrently taking digoxin, diuretics, or other drugs associated
with hypomagnesemia
Reference - FDA MedWatch 2011 Mar 2
hypomagnesemia reported in patients taking pyridylmethylsulphonyl
benzimidazadole derivative proton pump inhibitors (level 3 [lacking direct]
evidence)
based on systematic review of case reports
systematic review of 5 case reports and 6 case series evaluating hypomagnesemia in
28 patients (median age of diagnosis 70 years) treated with PPI therapy
PPIs were all pyridylmethylsulphonyl benzimidazadole derivatives including
rabeprazole, esomeprazole, omeprazole, lansoprazole, and pantoprazole
all patients had diseases (such as previous bowel surgery, bacterial gastroenteritis)
or concomitant use of drugs (such as diuretics) that could contribute to

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 hypomagnesemia
61% had PPI treatment ≥ 5 years
29% had PPI treatment ≥ 10 years
plasma magnesium levels associated with symptoms (ranged from 0.12 mg/dL
[0.05 mmol/L] to 0.85 mg/dL [0.35 mmol/L])
plasma magnesium returned to normal after withdrawal of PPI in all patients
Reference - Curr Opin Gastroenterol 2011 Mar;27(2):180

Increased urinary excretion of magnesium

drugs that can increase excretion of magnesium include(1, 2)

diuretics including loop diuretics such as furosemide and distal tubule diuretics such as
thiazide
digoxin
antimicrobials (amphotericin B, aminoglycosides, foscarnet)
chemotherapeutic agents/immunosuppressants
cisplatin
targeted therapies (for example, cetuximab)
calcineurin inhibitors (tacrolimus, cyclosporine)
checkpoint inhibitors (Am J Nephrol 2017;45(2):160EBSCOhost Full Text)
for patients with epidermal growth factor (EGFR) inhibitor-induced
hypomagnesemia, resolution reported after discontinuation of EGFR-inhibitor (Clin
Colorectal Cancer 2016 Sep;15(3):e117)
severe hypomagnesemia reported in 3 patients receiving etoposide,
methylprednisolone, cytarabine, and cisplatin (ESHAP protocol) for non-Hodgkin
lymphoma in case series (BMC Blood Disord 2002;2(1):1 full-text)
mutations which affect proteins expressed in distal convoluted tubule and thick ascending limb
of the loop of Henle can alter magnesium homeostasis(3)
genetic causes of hypomagnesemia
Gitelman-like Hypomagnesemias:
Reported Estimated
Distinctive Clinical
Category/Name of Incidence or
Gene/Inheritance Findings in Addition
Disorder Estimated Number of
to Hypomagnesemia
Patients
SLC12A3 Chondrocalcinosis can
Gitelman syndrome 1 in 40,000
R develop later in life
Variable presentation
Autosomal dominant may include renal
tubulointerstitial HNF1B cysts, genital and
kidney disease/renal D 1 in 120,000
pancreatic

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 cysts and diabetes abnormalities,
including type II DM
Bartter syndrome, type BSND Renal failure early in
< 100 patients
4 R life possible
KCNJ10 Seizures, ataxia,
EAST syndrome < 50 patients
R sensorineural deafness
FXYD2 < 50 patients (from 3
IDH NA
D families)
HPABH4D/RCAD- PCBD1 MODY5-like
< 50 patients
like R presentation
Abbreviations: D, dominant; DM, diabetes mellitus; EAST, epilepsy, ataxia, sensorineural
deafness, and tubulopathy; HPABH4D, hyperphenylalaninemia BH4-deficient; IDH, isolated
dominant hypomagnesemia; MODY, maturity onset diabetes of the young; NA, not available;
R, recessive; RCAD, renal cysts and diabetes.Reference - (3).
Hypercalciuric Hypomagnesemias:
Reported Estimated
Distinctive Clinical
Category/Name of Incidence or
Gene/Inheritance Findings in Addition
Disorder Estimated Number of
to Hypomagnesemia
Patients
Renal failure,
CLDN16 polyuria/polydipsia,
FHHNC type 1 < 1,000 patients
R elevated serum intact
PTH
Same presentation as
CLDN19
FHHNC type 2 < 100 patients type 1 plus ocular
R
abnormalities
ADHH Bartter CASR Hypocalcemia plus
< 1,000 patients
syndrome type 5 D normal or low PTH
Sometimes Gitelman-
Bartter syndrome, type CLCNKB
< 1,000 patients like phenotype, rarely
3 (classical type) R
nephrocalcinosis
Abbreviations: ADHH, autosomal dominant hypocalcemia with hypocalciuria; D, dominant;
FHHNC, familial hypomagnesemia with hypocalcemia and nephrocalcinosis; PTH, parathyroid
hormone; R, recessive.Reference - (3).
Mitochondrial Hypomagnesemias:
Reported Estimated
Incidence or Distinctive Clinical
Category/Name of
Gene/Inheritance Estimated Number of Findings in Addition
Disorder

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 Patients to Hypomagnesemia

Mitochondrial Retinopathy and

deletion cardiac conduction
KSS < 1,000 patients
Mitochondrial defects,
gene ophthalmoplegia
MT-T1
< 50 patients (from 1 Hypertension and
HHH mitochondrial
family) hypercholesterolemia
gene
Hyperuricemia,
SARS2 < 10 patients from 2 pulmonary
HUPRAS
R families hypertension, renal
failure, and alkalosis
Abbreviations: HHH, hypertension, hypercholesterolemia, and hypomagnesemia; HUPRAS,
hyperuricemia, pulmonary hypertension, renal failure, and alkalotic syndrome; KSS, Kearns-
Sayre syndrome; R, recessive.Reference - (3).
Other Hereditary Hypomagnesemias:
Reported Estimated
Distinctive Clinical
Category/Name of Incidence or
Gene/Inheritance Findings in Addition
Disorder Estimated Number of
to Hypomagnesemia
Patients
Severe
TRPM6 hypomagnesemia
HSH < 100 patients
R presenting in early
infancy
EGF 2 patients from 1
IRH Intellectual disability
R family
Severe inflammation
EGFR
NISBD2 1 patient of bowel and skin
R
presenting at birth
CNNM2 10 patients from 7 Seizures, intellectual
HSMR
D/R families disability
KCNA1 21 patients from 1
ADH/EA1 Episodic myokymia
D family
Hypocalcemic
FAM111A hypoparathyroidism,
KCS2 < 100 patients
D impaired skeletal
development

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 Abbreviations: ADH, autosomal dominant hypocalcemia; D, dominant; EA1, episodic ataxia
type 1; HSH, hypomagnesemia with secondary hypomagnesemia; HSMR, hypomagnesemia
with seizures and mental retardation; IRH, isolated recessive hypomagnesemia; KCS2, Kenny-
Chaffey syndrome type 2; NISBD2, neonatal inflammatory skin and bowel disease type 2; R,
recessive.Reference - (3).

Endocrine conditions associated with hypomagnesemia

endocrine conditions associated with hypomagnesemia include(2)

diabetes type 1 and type 2 (Rev Endocr Metab Disord. 2003 May;4(2):195)
hypercalcemia
hyperthyroidism
hungry bone syndrome after parathyroidectomy
hyperaldosteronism

Other causes

other causes of hypomagnesemia include(1, 2)

extracellular fluid volume expansion
recovery phase of acute tubular necrosis
severe burns
cardiopulmonary bypass surgery
excessive lactation, heat, prolonged exercise
mitral valve prolapse (MVP) (Magnes Res 2005 Mar;18(1):35)

Spurious laboratory results

pseudohypomagnesemia(1, 2)
collection of blood in potassium EDTA-containing sample tubes can cause spurious
hypomagnesemia
30% of magnesium is bound to albumin and is inactive; hypoalbuminemic states may
cause spurious hypomagnesemia because serum magnesium concentration is a measure of
total magnesium
red blood cell magnesium is generally higher than serum magnesium; avoid hemolysis when
measuring magnesium serum levels(2)

Pathophysiology
Normal physiologic function of magnesium

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 magnesium function and distribution in the body(2, 4)
magnesium is the second most abundant intracellular cation after potassium
magnesium is essential for numerous functions including
cofactor activity for > 300 enzymatic reactions
muscle contraction/relaxation
neurotransmission
cardiac conduction
platelet function such as clotting and/or thrombus formation
maintenance of vascular tone
platelet-activated thrombosis
bone formation
insulin regulation
magnesium shares chemical properties with calcium but has distinct biologic properties
and regulation
distribution
about 99% of total body magnesium is located in bone, muscles, and other soft
tissues
about 1% is found in the serum and includes
ionized magnesium (free)
protein bound magnesium
magnesium complexed with other anions (such as phosphate, sulfate, or
bicarbonate)
reported 85% of whole body magnesium does not exchange or does so very slowly
with an estimated half-life of 1,000 hours
myocardium, kidney parenchyma, fat tissue, skeletal muscle, brain tissue, and
lymphocytes have different rates of intracellular magnesium exchange
magnesium intake, absorption, and excretion(2)
daily recommended magnesium intake ≥ 310 mg for women and ≥ 400 mg for men
dietary sources rich in magnesium include green vegetables, nuts, seeds, and
unprocessed cereals
about 10% of daily intake comes from drinking water
magnesium is predominantly absorbed in small intestine with a smaller amount taken up
in the large intestine
24%-76% absorbed and remainder excreted in feces
absorption is determined by magnesium status (increased absorption when
magnesium levels are low and vice versa), not by intake
kidneys are important for maintaining magnesium homeostasis
renal excretion can vary from 0.5% to 70% of filtered load depending on
magnesium balance
about 2,400 mg magnesium are filtered daily

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 95% of filtered load is immediately reabsorbed (60%-70% in the ascending limb of
loop of Henle and 10% via distal tubules), and 3%-5% excreted (about 100 mg) is
excreted in urine

Pathogenesis of acquired hypomagnesemia

hypomagnesemia can result from(1, 2)

decreased dietary intake usually accompanied by severe or prolonged diarrhea (Rev
Endocr Metab Disord. 2003 May;4(2):195)
urinary wasting
redistribution of magnesium from extracellular to intracellular compartment
because magnesium has many essential biological roles, deficiency results in varied clinical
manifestations(2)
neuromuscular irritability (weakness, muscle fasciculations, tetany, or seizures) is caused
by disruption in muscle contraction/relaxation and neurotransmission
cardiovascular manifestations (arrhythmias) are caused by reduced intracellular potassium
levels induced by hypomagnesemia
magnesium is an essential cofactor for the cell membrane pump that drives
potassium into cells in exchange for sodium at the cost of adenosine triphosphate
(sodium-potassium ATPase)
additionally, in the myocardium, magnesium mediates closure of specific potassium
channels
when magnesium is deficient, intracellular potassium levels drop, reducing the
threshold for generating an action potential in the cardiac myocyte
reduced intracellular potassium levels also prolong time to repolarize the cell
membrane (flow of potassium out of the cell is slower)
Reference - Rev Endocr Metab Disord. 2003 May;4(2):195
magnesium deficiency can cause other electrolyte deficiencies(1)
hypocalcemia can occur, because hypomagnesemia
impairs response of parathyroid gland to release parathyroid hormone in the
presence of low calcium levels
causes end-organ resistance to parathyroid hormone action
causes reduced 1,25 vitamin D levels (results from low parathyroid hormone levels
and decreased renal conversion of 25-hydroxyvitamin D to 1,25 vitamin D) (Rev
Endocr Metab Disord. 2003 May;4(2):195)
hypokalemia
may occur due to common underlying etiologies that increase magnesium and
potassium secretion
may result when hypomagnesemia eliminates inhibition of renal outer medullary
potassium channels that secrete potassium in to the urinary space (J Am Soc

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 Nephrol 2007 Oct;18(10):2649 full-text)

Pathogenesis of inherited hypomagnesemias

inherited hypomagnesemias (3)

encoded proteins of affected genes are all known and are all expressed in distal
convoluted tubule (DCT) or thick ascending limb of Henle (TAL)
exact molecular mechanism of some of the genetic disorders is not fully elucidated
pathogenesis by type of inherited hypomagnesemia(3)
Gitelman-like hypomagnesemias
mutations found in these disorders affect transport of sodium, potassium, and/or
chloride in the DCT
transcellular reabsorption of magnesium in the DCT depends on the apical
membrane potential
when transport of other ions is disrupted, the membrane potential is altered and
impacts transport of magnesium
Gitelman-like hypomagnesemias cause increased calcium reabsorption and
subsequent hypocalciuria and fluid loss with tendency to lower blood pressure
renin-angiotensin-aldosterone system is activated via fluid loss, and increased
aldosterone causes secretion of potassium in exchange for sodium and subsequent
hypokalemia
combination of hypokalemia and hypomagnesemia can result in cardiac
arrhythmias and prolonged QT intervals on electrocardiogram
Pathogenesis of Gitelman-like Hypomagnesemias:
Affected Gene and
Name of Disorder Protein Function
Protein Name
SLC12A3 Thiazide-sensitive NaCl
Gitelman syndrome
NCC cotransporter
Subunit of chloride
BSND channel Kb and Ka,
Bartter syndrome, type 4
Barttin expressed in TAL, DCT,
and inner ear
K+ channel that promotes
KCNJ10 outward K+ currents to
EAST syndrome
Kir4.1 counter K+ imported by
Na+/K+-ATPase
FXYD2 Gamma subunit increases
Gamma subunit of affinity of Na+/K+-ATPase
IDH Na+/K+- for ATP and decreases its

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 ATPase affinity for Na+ and K+
Transcription factor;
mutations in HNF1B can
disrupt normal
Autosomal dominant
development of kidney,
tubulointerstitial kidney HNF1B
pancreas, and genital tract;
disease/renal cysts and HNF1beta
HNF1B dysfunction
diabetes
causes decreased
transcription of specific
splice-form of FXYD2
Dimerization factor that
PCBD1
HPABH4D/RCAD-like regulates transcription of
PCBD1
HNF1a and HNF1b
Abbreviations: ATP, adenosine triphosphate; ATPase, adenosine triphosphatase;
DCT, distal convoluted tubule; EAST, epilepsy, ataxia, sensorineural deafness, and
tubulopathy; HPABH4D, hyperphenylalaninemia BH4-deficient; IDH, isolated
dominant hypomagnesemia; K+, potassium; Na+, sodium; RCAD, renal cysts and
diabetes; TAL, thick ascending limb of Henle. Reference - (3), Nephrol Dial
Transplant 2015 Jun;30(6):952.
hypercalciuric hypomagnesemias
mutations found in these disorders affect reabsorption of calcium and magnesium
ions in the TAL
reabsorption of calcium and magnesium via paracellular transport pathways require
the lumen-positive transepithelial potential difference
when the voltage difference or paracellular pathway is disrupted, transport of
calcium and magnesium is impaired
hypercalciuric hypomagnesemias can cause nephrocalcinosis or chronic kidney
disease
Pathogenesis of Hypercalciuric Hypomagnesemias:
Affected Gene and
Name of Disorder Protein Function
Protein
Component of tight
CLDN16 junction; mutated protein
FHHNC type 1
Claudin-16 disrupts pore selectivity of
tight junction
Component of tight
junction expressed in
CLDN19 kidney and retina; mutated
FHHNC type 2
Claudin-19 protein causes renal and

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 ocular anomalies
Ca2+ sensing receptor;
mutated protein suppresses
CASR
ADHH* salt reabsorption and
CaSR
disrupts tight junction pore
selectivity
Cl- ion channel that
provides exit pathway for
CLCNKB
Bartter syndrome type 3 chloride ions; mutations
Clc-Kb
disrupts intracellular
chloride level
Abbreviation: ADHH, autosomal dominant hypocalcemia with hypocalciuria;
Ca2+, calcium; Cl-, chloride; FHHNC, familial hypomagnesemia with
hypocalcemia and nephrocalcinosis.* Also known as Bartter syndrome type
5.Reference - (3).
mitochondrial hypomagnesemias
pathophysiological mechanism of each type is not fully understood
phenotype depends on both the mutation and the fraction of mitochondria affected
in each tissue
genetic aberrations include deletions in mitochondrial genome (Kearns-Sayre
syndrome), mutations in mitochondrial gene MT-T1, and recessive mutations in
SARS2
other hypomagnesemias
heterogeneous group with varying mechanisms, only some of which are understood
includes disorders caused by mutations in the distal convoluted tubule- and colon-
specific apical magnesium channel gene (TRPM6) and mutations in the genes that
affect the activity and expression of this channel

General Evaluation
Clinical presentation

most patients are asymptomatic until serum magnesium concentration is < 1.2 mg/dL (0.5
mmol/L), but some patients remain asymptomatic even with severe hypomagnesemia(1, 2)
presentation may overlap with that of other biochemical abnormalities frequently associated
with hypomagnesemia including(1)
hypokalemia (reported in up to 60% of cases)
hypocalcemia
early presentation of hypomagnesemia includes(2)

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 nausea
vomiting
loss of appetite
fatigue and weakness
worsening deficiency associated with symptoms of(2)
numbness
muscle tingling, contractions, and cramps
presentation of severe hypomagnesemia (< 1 mg/dL [0.4 mmol/L]) may include(1)
seizures
drowsiness
confusion
coma
symptoms affecting the central nervous system include depression, agitation, psychosis,
nystagmus, seizures, and sudden changes in behavior(2)
presentation may include cardiac symptoms including(1, 2)
atrial arrhythmias
ventricular arrhythmias (may be life-threatening)
intermittent downbeat nystagmus, cerebellar ataxia, generalized convulsions, and a
supraventricular tachycardia in 59-year-old man with severe hypomagnesemia in case report
(Biol Trace Elem Res 2011 Aug;142(2):127EBSCOhost Full Text)
hypomagnesemia induced seizures in 73-year-old woman after ileal resection and limited right
hemicolectomy for small bowel volvulus in case report (BMJ Case Rep 2009;2009 full-text)

History

patients may complain of(1, 2, 4)

nausea
vomiting
fatigue
muscular weakness, twitching, cramps, or numbness
dysphagia
symptoms affecting the central nervous system including
depression and/or apathy
agitation
delirium
tremor
paraesthesia
seizures
sudden changes in behavior
ask about use of(1, 2)

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 proton pump inhibitors
diuretics
antimicrobial medications
chemotherapeutic agents/immunosuppressants
laxatives
see causes for specific drugs
ask about medical and surgical history including(1, 2, 4)
diarrhea and/or vomiting
kidney disease
alcohol use disorder
anorexia nervosa
parenteral nutrition
diabetes (type 1 and type 2)
small bowel bypass surgery
parathyroid disease and parathyroidectomy
hyperaldosteronism
ask about family history of(3)
hypomagnesemia
hypokalemia
kidney disease
diabetes mellitus, including maturity onset diabetes of the young (MODY) 5 (HNF1B
mutation) (Am J Nephrol 2015;42(1):85EBSCOhost Full Text full-text)

Physical Exam

look for
vertical nystagmus(1)
tetany (may be attributed to coexisting metabolic abnormalities) indicated with positive(1)
Chvostek sign (tapping on facial nerve leading to twitching of facial muscles)
Trousseau sign (carpopedal spasm with inflated blood pressure cuff)
Reference - BMJ 2008 Jun 7;336(7656):1298 full-text
tremors(1)
muscular fasciculation(2)
seizures (in severe cases)(1, 2, 4)

Additional Testing
Testing overview

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 hypomagnesemia is defined as serum magnesium concentration < 1.8 mg/dL (0.75 mmol/L);
reference range varies between laboratories, and lower limit of normal may be defined as low as
< 1.5 mg/dL (0.62 mmol/L)
once hypomagnesemia is established, perform urine studies to differentiate renal vs.
gastrointestinal losses
calculate fractional excretion of magnesium on spot urine
consider measurement of 24-hour urinary magnesium excretion (rarely performed)
consider performing electrocardiogram in patients with unexplained arrhythmias
consider genetic testing if inherited hypomagnesemia is suspected (positive family history,
hypomagnesemia without other explanation or hypomagnesemia that is discovered in infancy)

Laboratory evaluation

Blood tests

interpreting serum magnesium concentration

hypomagnesemia is defined as serum magnesium concentration < 1.8 mg/dL (0.75
mmol/L); reference range varies between laboratories, and lower limit of normal may be
defined as low as < 1.5 mg/dL (0.62 mmol/L)((1, 2, 4), QJM 2016 Jul;109(7):453)
precautions and limitations of using serum magnesium for diagnosis of magnesium
deficiency(1, 2)
may not adequately reflect total body status because < 1% of total magnesium is
found in blood
red blood cell magnesium is generally higher than serum magnesium, so it is
important to avoid hemolysis when measuring magnesium serum levels
collection of blood in potassium-EDTA, a common sample tube anticoagulant, can
cause spurious hypomagnesemia
30% of magnesium is bound to albumin and is inactive; hypoalbuminemic states
may cause spurious hypomagnesemia, because serum magnesium concentration is a
measure of total magnesium
no clinically available "ionized" magnesium test to diagnose deficiency based on free
magnesium(4)
DynaMed commentary – basic metabolic profile is usually obtained first or at the same time
(includes sodium, potassium, chloride, bicarbonate, creatinine, and blood urea nitrogen; usually
also includes glucose and calcium measurements)

Urine studies

once low serum magnesium level is established, to differentiate renal vs. gastrointestinal losses,
calculate fractional excretion of magnesium (FEMg) on spot urine or consider obtaining 24-hour

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 urinary magnesium excretion(1, 2)
see DynaMed calculator for Fractional Excretion of Magnesium; see also Fractional
Excretion of Magnesium (SI units) (requires creatinine and magnesium measurements
from both serum and urine for calculation)
24-hour urinary magnesium excretion requires complete 24-hour collection of specimen
for accurate assessment of magnesium excretion (rarely performed)
Interpreting Urine Studies of Hypomagnesemia:
Result Indicates Renal Result Indicates GI Losses
Urine Test
Wasting +/- Reduced Intake
FEMg > 2% < 2%
24-hour urinary excretion High (> 24 mg [1 mmol]) Low (< 12 mg [0.5 mmol])
Abbreviations: FEMg, fractional excretion of magnesium; GI, gastrointestinal. Reference
- (1).
indirect measurement of intracellular magnesium by magnesium infusion test is only useful if
there is strong clinical suspicion of deficiency in patients with normal serum magnesium(1)

Genetic testing

approach to genetic testing if inherited hypomagnesemia is suspected (positive family history,

hypomagnesemia without other explanation, or hypomagnesemia that is discovered in infancy)
(3)

assess for Gitelman-like phenotype including any of

marked hypocalciuria
loss of sodium and potassium
low blood pressure due to water loss
cardiac arrhythmias and prolonged QT interval on electrocardiogram
if patient has hypomagnesemia accompanied with Gitelman-like phenotype
and if extrarenal symptoms are present, consider genetic testing for
Gene/Disorder Name Clinical Features
Early renal failure, prenatal
BSND (Bartter syndrome type 4)
complications
KCNJ10 (EAST syndrome) Seizures, sensorineural deafness
HNF1B (ADTKD/RCAD) MODY, genital and renal anomalies
PCBD1 (HPABH4D/RCAD-like) MODY
Mitochondrial hypomagnesemias Variable
Abbreviations: ADTKD, autosomal dominant tubulointerstitial kidney disease;
EAST, epilepsy, ataxia, sensorineural deafness, and tubulopathy; HPABH4D,
hyperphenylalaninemia BH4-deficient; MODY, mature onset diabetes of the

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 young; RCAD, renal cysts and diabetes.
and if no extrarenal symptoms are present, consider genetic testing for
SLC12A3 (Gitelman syndrome)
FXYD2 (isolated dominant hypomagnesemia)
CLCNKB (Bartter syndrome type 3 [classical type])
if patient has hypomagnesemia without Gitelman-like phenotype
and if hypercalciuria is present, consider genetic testing for
Gene/Disorder Name Clinical Features
CLDN16 (FHHNC type 1) No distinctive features
CLDN19 (FHHNC type 2) Ocular abnormalities
CASR (ADHH) Normal to low PTH
May progress to Gitelman-like
CLCNKB (Bartter syndrome, type 3)
phenotype
Mitochondrial hypomagnesemias Variable
Abbreviations: ADHH, autosomal dominant hypocalcemia with hypocalciuria;
FHHNC, familial hypomagnesemia with hypocalcemia and nephrocalcinosis;
PTH, parathyroid hormone.
and if concentration of urinary calcium is normal, consider genetic testing for
Gene (Disorder Name) Clinical Features
Serum magnesium < 0.5 mg/dL (0.2
TRPM6 (HSH)
mmol/L)
CNNM2 (HSMR) Intellectual disability
EGF (IRH) Intellectual disability
EGFR (NISBD2) Inflamed bowel and skin
KCNA1 (ADH/EA1) Episodic myokymia
FAM111A (KCS2) Impaired skeletal development
Abbreviations: ADH, autosomal dominant hypomagnesemia; EA1, episodic ataxia
type; HSH, hypomagnesemia with secondary hypomagnesemia; HSMR,
hypomagnesemia with seizures and mental retardation; IRH, isolated recessive
hypomagnesemia; KCS2, Kenny-Chaffey syndrome type 2; NISBD2, neonatal
inflammatory skin and bowel disease type 2.

Electrocardiography

consider performing electrocardiogram in patients with unexplained arrhythmias;

hypomagnesemia-induced changes include(1)
flattened T-waves and U-waves

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 prolonged QT interval and widened QRS complexes

Management
Management overview

treatment depends on severity of deficiency

for severe or symptomatic hypomagnesemia, give IV magnesium sulfate with treatment
goal of serum magnesium concentration > 1 mg/dL (0.411 mmol/L)
for patients with asymptomatic hypomagnesemia, consider oral magnesium
supplementation preferably with sustained-release magnesium if available
if present, treat concomitant hypokalemia and/or hypocalcemia; see also hypokalemia
consider use of potassium-sparing diuretics for patients who cannot discontinue diuretics

Medications

Oral magnesium

oral magnesium supplements typically reserved for asymptomatic patients

sustained release magnesium preparations(1)
diarrhea typically associated with standard magnesium preparations may be reduced
options include
magnesium chloride contains 64-71.5 mg elemental magnesium (trade
names; Slo-Mag, Mag Delay)
magnesium L-lactate contains 84 mg elemental magnesium (Mag-Tab SR)
Reference - Int J Nephrol Renovasc Dis 2014;7:219 full-text
standard magnesium preparation(1, 2)
generally not well-absorbed from gastrointestinal tract and may cause diarrhea
if patient is intolerant of 1 particular magnesium salt or if it is found to be
ineffective, try a different magnesium salt
preparations typically provide 60-96 mg (2.5-3.5 mmol) magnesium per tablet
dosing
for asymptomatic patients, 2-4 tablets daily
for severe depletion, 6-8 tablets daily in divided doses
for chronic hypomagnesemia, high doses > 10 mg/kg/day (Panminerva Med
2001 Sep;43(3):177)

Injectable magnesium

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 IV magnesium sulfate(1, 2, 4)
typically reserved for symptomatic patients or when immediate correction is required,
such as patients with ventricular arrhythmia
consider IV magnesium sulfate over oral supplements for patients with gastrointestinal
disorders
1 g magnesium sulfate is equivalent to 100 mg (4 mmol) of elemental magnesium
given as 20% solution (commercially available 50% solution containing 0.5 g/mL [2
mmol/mL] magnesium sulfate should be diluted with 0.9% sodium chloride or 5%
glucose)
treatment goal is serum magnesium > 1 mg/dL (0.4 mmol/L)
suggested regimen based on consensus opinion
magnesium sulfate 8-12 g IV for first 24 hours
magnesium sulfate 4-6 g/day IV for 3-4 additional days
infusion rate should not exceed 2 g/hour to minimize urinary excretion
in patients with renal insufficiency, give 25%-50% of recommended initial dose
in elderly patients or those receiving high doses, monitor with electrocardiogram
intramuscular magnesium(1)
administration is painful; should be reserved for urgent conditions or patients with no IV
access
dose ranges from magnesium sulfate 1-2 g intramuscularly every 6 hours for 24 hours
given as 50% solution

Other medications

in patients with hypocalcemia, treat with calcium before initiating magnesium replacement
(sulfate from magnesium sulfate can complex with ionized calcium resulting in increased
urinary excretion of calcium) (Emerg Med Clin North Am 2014 May;32(2):349)
in patients with chronic renal magnesium wasting or diuretic-induced hypomagnesemia (who
cannot discontinue diuretic therapy), consider addition of potassium-sparing diuretic such as
amiloride or triamterene(1)

Complications and Prognosis

Complications

other electrolyte deficiencies(1, 2, 3)

hypokalemia reported in 40%-60% of patients with hypomagnesemia
hypocalcemia - classical sign of severe hypomagnesemia
exacerbation of digitalis toxicity (Rev Endocr Metab Disord. 2003 May;4(2):195 )

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 ventricular or atrial arrhythmias (especially with concomitant hypokalemia)(1, 2, 3)
chondrocalcinosis(3)

Prognosis

mortality in adults
hypomagnesemia associated with increased mortality, length of ICU stay, and need
for mechanical ventilation in critically ill patients
based on systematic review of observational studies
systematic review of 6 cohort studies evaluating association between magnesium
status and prognosis in 1,550 critically ill patients
serum magnesium measurement was performed either upon admission or within 24
hours of admission to hospital or intensive care unit (ICU)
cutoffs used for defining hypomagnesemia in studies ranged from < 1.5 mg/dL
(0.62 mmol/L) to < 1.8 mg/dL (0.74 mmol/L)
hypomagnesemia associated with increased
mortality (risk ratio [RR] 1.9, 95% CI 1.48-2.44) in analysis of 6 studies with
1,550 patients, results limited by significant heterogeneity
mechanical ventilation requirement (RR 1.65, 95% CI 1.12-2.43) in analysis
of 3 studies with 801 patients, results limited by significant heterogeneity
length of ICU stay (mean difference of 4.1 days, 95% CI 1.16-7.04) in
analysis of 3 studies with 974 patients
Reference - QJM 2016 Jul;109(7):453
hypomagnesemia associated with increased risk of continued renal failure and in-
hospital mortality in patients with AIDS and acute kidney injury
based on prospective cohort study
54 patients (aged > 18 years, 72% male) hospitalized with HIV infection and acute
renal injury had assessment of serum magnesium and were followed for length of
hospital stay
principal causes of renal failure were treatment with nephrotoxic drugs (65%),
sepsis (48%), and dehydration (32%)
33% had hypomagnesemia (< 1.7 mg/dL [0.7 mmol/L]), 33% recovered renal
function, and 44% died during hospital stay
in multivariable analysis, hypomagnesemia associated with increased risk of
nonrecovery of renal function (adjusted odds ratio [OR] 6.94, 95% CI 1.2-
39.9)
in-hospital mortality (adjusted OR 6.92, 95% CI 1.17-40.8)
Reference - Braz J Med Biol Res 2010 Mar;43(3):316 full-text
hypomagnesemia at admission to intensive care unit associated with increased risk of
mortality in patients with type 2 diabetes

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 based on prospective cohort study
14 adults (median age 55.5 years) with type 2 diabetes admitted to ICU had serum
magnesium assessed and were followed for length of ICU stay
72% had hypomagnesemia (< 1.6 mg/dL [0.66 mmol/L]) at admission
hypomagnesemia associated with increased mortality compared to normo-
magnesemia (adjusted odds ratio, 1.9, 95% CI 1.2-14.7)
Reference - Magnes Res 2008 Sep;21(3):163 full-text
inconsistent evidence for impact of hypomagnesemia on mortality in children in intensive care
hypomagnesemia not associated with increased mortality or longer hospitalization in
critically ill children
based on retrospective cohort study
179 children aged 1 month to 15 years admitted to pediatric intensive care unit
(PICU) with record of serum magnesium had review of medical record
44% had hypomagnesemia
overall mortality 30%
no significant difference between hypomagnesemia and normo-magnesemia in
mortality or length of hospitalization
Reference - Indian J Pediatr 2009 Dec;76(12):1227EBSCOhost Full Text
hypomagnesemia associated with increased mortality in critically ill children
based on prospective cohort study
100 children aged 6 months to 12 years admitted to PICU had blood drawn on
admission and on alternate days for evaluation of electrolytes including serum
magnesium
60% had hypomagnesemia (≤ 1.7 mg/dL [0.7 mmol/L])
mortality in children with hypomagnesemia 30% vs. 3.3% in children with normal
magnesium levels (p < 0.05)
Reference - J Trop Pediatr 2003 Apr;49(2):99EBSCOhost Full Text
hypomagnesemia associated with increased hospital stay length and discharge to care
facility in patients admitted to hospital
based on retrospective cohort study
65,974 adults (mean age 62 years) admitted to Mayo Clinic (Rochester, Minnesota) were
assessed for serum magnesium alterations
20% had hypomagnesemia (< 1.7 mg/dL [0.7 mmol/L])
clinical outcome analysis adjusted for age, sex, estimated glomerular filtration rate,
comorbidity, and principal diagnosis
compared to serum magnesium 1.7-1.89 mg/dL (0.7-0.8 mmol/L) in adjusted analysis
hypomagnesemia associated with
increased relative length of hospital stay
adjusted odds ratio (OR) 1.17, 95% CI 1.14-1.2 (for serum magnesium
1.5-1.69 mg/dL [0.6-0.7 mg/dL])
adjusted OR 1.38, 95% CI 1.35-1.42 (for serum magnesium < 1.5

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 mg/dL [0.6 mmol/L])
increased discharge to a care facility
adjusted OR 1.09, 95% CI 1.01-1.18 (for serum magnesium 1.5-1.69
mg/dL [0.6-0.7 mg/dL])
adjusted OR 1.21, 95% CI 1.1-1.33 (for serum magnesium < 1.5 mg/dL
[0.6 mmol/L])
no significant difference in mortality for serum magnesium ≤ 1.69 mg/dL (0.7
mmol/L)
Reference - Mayo Clin Proc 2015 Aug;90(8):1001 full-text

Prevention and Screening

Prevention

guidance from the FDA regarding proton pump inhibitor treatment in patients who are taking
other drugs known to cause hypomagnesemia including digoxin and diuretics
consider obtaining baseline serum magnesium level before starting proton pump inhibitor
treatment
consider periodic monitoring of serum magnesium
Reference - FDA MedWatch 2011 Mar 2
IV magnesium sulfate 50 mg/kg during rewarming phase of bypass surgery may reduce
hypomagnesemia and junctional ectopic tachycardia in children having cardiac surgery
(level 2 [mid-level] evidence)
based on small randomized trial
99 children having cardiac surgery randomized to magnesium sulfate 50 mg/kg IV vs.
magnesium sulfate 25 mg/kg IV vs. placebo during rewarming phase of cardiopulmonary
bypass
comparing magnesium 50 mg/kg vs. magnesium 25 mg/kg vs. placebo
hypomagnesemia after surgery, at admission to cardiac intensive care unit in 47.4%
vs. 63% vs. 77.8% (p < 0.05 for 50 mg/kg vs. placebo)
junctional ectopic tachycardia in 0% vs. 6.7% vs. 17.9% (p = 0.009 for combined
magnesium groups vs. placebo)
Reference - J Thorac Cardiovasc Surg 2010 Jan;139(1):162 full-text

Guidelines and Resources

Review articles

review can be found in Int J Nephrol Renovasc Dis 2014;7:219 full-text

review of proton pump inhibitor-induced hypomagnesemia can be found in World J Nephrol

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 2016 Mar 6;5(2):152 full-text
review of hypomagnesemia due to targeted antiepidermal growth factor receptor (EGFR) agents
can be found in Target Oncol 2011 Dec;6(4):227EBSCOhost Full Text
review of physiology of magnesium, calcium, phosphate, and vitamin D can be found in Endocr
Dev 2015;28:7
review of refeeding syndrome can be found in Dimens Crit Care Nurs 2009 Mar-Apr;28(2):53
review of refeeding syndrome can be found in BMJ 2008 Jun 28;336(7659):1495 full-text
case presentation of hypomagnesemia induced by several proton pump inhibitors can be found
in Ann Intern Med 2009 Nov 17;151(10):755EBSCOhost Full Text, correction can be found in
Ann Intern Med 2010 Feb 16;152(4):268
case presentation of refractory hypomagnesemia in 2 patients taking omeprazole can be found in
BMJ 2008 Jul 10;337:a425 full-text
case report of hypomagnesemia associated with chronic proton pump inhibitor use can be found
in Arch Intern Med 2011 Aug 8;171(15):1391EBSCOhost Full Text

MEDLINE search

to search MEDLINE for (Hypomagnesemia) with targeted search (Clinical Queries), click
therapy, diagnosis, or prognosis

Patient Information
information on hypomagnesemia with secondary hypocalcemia from Genetics Home Reference
of the United States Library of Medicine
handout low magnesium level from Medline Plus or in Spanish

References
General references used

1. Ayuk J, Gittoes NJ. How should hypomagnesaemia be investigated and treated? Clin
Endocrinol (Oxf). 2011 Dec;75(6):743-6
2. Jahnen-Dechent W, Ketteler M. Magnesium basics. Clin Kidney J. 2012 Feb;5(Suppl 1):i3-
i14 full-text
3. Viering DHHM, de Baaij JHF, Walsh SB, Kleta R, Bockenhauer D. Genetic causes of
hypomagnesemia, a clinical overview. Pediatr Nephrol. 2017 Jul;32(7):1123-1135EBSCOhost
Full Text full-text
4. Moe SM. Disorders involving calcium, phosphorus, and magnesium. Prim Care. 2008
Jun;35(2):215-37, v-vi full-text

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Special acknowledgements

Brad Denker, MD (Associate Professor of Medicine, Harvard Medical School; Clinical Director,
Renal Division, Beth Israel Deaconess Medical Center; Massachusetts, United States)
Dr. Denker declares no relevant financial conflicts of interest.

Esther Jolanda van Zuuren, MD (Head of Allergy, Dermatology, and Venereology, Leiden
University Medical Centre; Netherlands; Editor, Cochrane Skin Group)
Dr. van Zuuren declares no relevant financial conflicts of interest.

William Aird, MD (Deputy Editor of Hematology, Endocrinology, and Nephrology; Professor of

Medicine, Harvard Medical School; Massachusetts, United States)
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DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 - . Record No.
T113769, Hypomagnesemia - approach to the patient; [updated 2018 Nov 30, cited place cited
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