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Magnesium, Urine Random (UMGR)

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EPIC Test Name

MAGNESIUM, URINE

EPIC Code

LAB405

Specimen Requirements

Urine
Minimum Volume:1.0 mL
Collection:Collect using standard laboratory procedures
Transport:Room Temperature ASAP
Stability:Room Temperature: 3 days at 15-25 degrees C Refrigerated: 3 days at 2-8 degrees C
Container:Urine cup
Processing/Storage:Acidify with 6M HCL after collection.
Rejection Causes:Insufficent Sample Volume
Samples perservered in Boritex

Methods

Colorimetric endpoint

Turnaround Time

SpecimenTurnaround TimeFrequency
UrineRoutine: 4 hours24/7

Reference Ranges

Colorimetric endpoint
All Range
Not established

Clinical Indications

Magnesium, the second (after potassium) most dominant intracellular cation, functions as a cofactor for > 300 enzymes, e.g., all adenosine triphosphate (ATP)-dependent enzymatic activities require magnesium as a cofactor. Magnesium also affects neurotransmitter release by competitively inhibiting the calcium entry into presynaptic nerve terminals. Thus, Mg deficiency can cause a variety of metabolic abnormalities and increased neuromuscular excitability.
Extracellularly, Mg accounts for about 1% of the total body magnesium content. About 55% of the plasma Mg exists in free form, 30% is associated with proteins (primarily albumin), and 15% is complexed with anions, e.g., phosphate and citrate.
The plasma magnesium levels, similar to potassium, are regulated to maintain within a narrow range mainly at the ascending loop of Henle in the kidneys.
Hypomagnesemia can be caused via renal or/and fecal magnesium wasting, e.g., congenital defects (including Barter and Gitelman syndrome), various endocrine disorders (including hyperaldosteronism and hyperparathyroidism), exposure to certain drugs (ie, diuretics, cis-platinum, aminoglycoside antibiotics, calcineurin inhibitors), and other miscellaneous causes (including chronic alcohol abuse), fat malabsorption and chronic diarrhea.
Hypermagnesemia can occur to patients with acute and chronic renal failure, magnesium overload, and condition causing magnesium release from the intracellular space. In consequence, for patients with mild-to-moderate hypermagnesemia, a prolong atrioventricular conduction time may occur. Magnesium toxicity may cause depression, cardiac arrest, and respiratory arrest.

Additional Information

Caution must be exercised in interpretation of results for patients with intravenous magnesium infusion.

Performed

Lab
Chemistry - Downtown

Interpretative Information

Interpretation of urinary magnesium levels should be in concert with serum Mg concentrations.
For patients with hypomagnesemia, random urine magnesium values greater than the upper limit of the reference range suggests renal magnesium wasting, whereas, lower values suggest inadequate magnesium intake and/or gastrointestinal losses.
For patients with hypermagnesemia, urinary magnesium concentrations provides information on current magnesium intake.
Low levels of urinary magnesium excretion increase urinary calcium oxalate and calcium phosphate supersaturation and could increase the risk of kidney stone formation.

CPT

83735

LOINC

19124-7

References

1. Liebman M, Costa G. Effects of calcium and magnesium on urinary oxalate excretion after oxalate loads. J Urol. 2000 May;163(5):1565-9. PMID: 10751889.
2. Johansson G, Backman U, Danielson BG, Fellström B, Ljunghall S, Wikström B. Effects of magnesium hydroxide in renal stone disease. J Am Coll Nutr. 1982;1(2):179-85. doi: 10.1080/07315724.1982.10718985. PMID: 6764473.

Contact Information

Chemistry - Downtown: (315)464-4460
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