Sorted By Test Name - Mayo Medical Laboratories

MGF
81345
MGRU
60245
diuretics) enhance excretion, resulting in high output of magnesium.
Reference Values:
0-15 years: not established
> or =16 years: 75-150 mg/specimen
Clinical References: 1. Fentona TR, Eliasziw M, Lyon SC, et al: Low 5-year stability of
within-patient ion excretion and urine pH in fasting-morning-urine specimens. Nutr Res 2009;29:320-326
2. Mircetic RN, Dodig S, Raos M, et al: Magnesium concentration in plasma, leukocytes and urine of
children with intermittent asthma. Clin Chim Acta 2001;312:197-203
Magnesium, Random, Feces
Clinical Information: Magnesium is a normal constituent in the diet and is normally present in fecal
material. Magnesium is also a commonly used laxative that can be the cause of chronic diarrhea. Sodium,
potassium, chloride, and sulfate are usually the major contributors to fecal osmolality. Fecal osmolality is
normally 2 x (sodium + potassium) unless there are exogenous factors inducing a change in this ratio,
such as the presence of other osmotic agents (magnesium sulfate, saccharides), or drugs inducing
secretions, such as phenolphthalein or bisacodyl. If magnesium is excreted at a high rate (>200 mEq/kg),
with an osmotic gap >100 mOsm/kg, magnesium is likely to be the principle contributor to osmotic
diarrhea. Use of magnesium salts in the form of over-the-counter stool softeners is the most likely source
of such excess excretion.
Useful For: Diagnosis of osmotic diarrhea due to excessive ingestion of magnesium Ruling out
excessive ingestion of magnesium in the work-up of chronic diarrhea
Interpretation: The osmotic theory of diarrhea is explained by the equation: 2x (stool sodium + stool
potassium) = stool Osmolality + or - 30 mOsm. Normal fecal sodium and potassium in the presence of an
osmotic gap (>30 mOsm/kg) suggests osmotic diarrhea. Increased concentration of fecal magnesium
contributes to osmotic diarrhea. Magnesium concentration of >200 mEq/kg is frequently associated with
decreased fecal sodium and potassium, and is an indicator of excessive consumption of magnesium that is
likely the cause of diarrhea.
Reference Values:
0-15 years: not established
> or =16 years: 0-199 mEq/kg
Clinical References: 1. Phillips S, Donaldson L, Geisler K, et al: Stool composition in factitial
diarrhea: a 6-year experience with stool analysis. Ann Intern Med 1995;123:97-100 2. Ho J, Moyer T,
Phillips S: Chronic diarrhea: the role of magnesium. Mayo Clin Proc 1995;70:1091-1092 3. Fine KD,
Santa Ana CA, Fordtran JS: Diagnosis of magnesium-induced diarrhea. N Engl J Med
1991;324:1012-1017
Magnesium, Random, Urine
Clinical Information: Magnesium, along with potassium, is a major intracellular cation. Magnesium
is a cofactor of many enzyme systems. All adenosine triphosphate (ATP)-dependent enzymatic reactions
require magnesium as a cofactor. Approximately 70% of magnesium ions are stored in bone. The
remainder is involved in intermediary metabolic processes; about 70% is present in free form, while the
other 30% is bound to proteins (especially albumin), citrates, phosphate, and other complex formers. The
serum magnesium level is kept constant within very narrow limits. Regulation takes place mainly via the
kidneys, primarily in the ascending loop of Henle. Conditions that interfere with glomerular filtration
result in retention of magnesium and, hence, elevation of serum concentrations. Hypermagnesemia is
found in acute and chronic renal failure, magnesium overload, and magnesium release from the
intracellular space. Mild-to-moderate hypermagnesemia may prolong atrioventricular conduction time.
Magnesium toxicity may result in central nervous system (CNS) depression, cardiac arrest, and
respiratory arrest. Numerous studies have shown a correlation between magnesium deficiency and
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