Serum Sodium 

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Measurement of serum sodium is routine in assessing electrolyte, acid-base, and balance, as well as renal function. Sodium accounts for approximately 95% of the osmotically active substances in the extracellular compartment, provided that the patient is not in renal failure or does not have severe hyperglycemia. 

The reference range for serum sodium is 135-147 mmol/L, [1]  although different assays establish their own reference ranges, which may differ slightly. For the Architect c System that runs integrated chip technology (ICT) sodium, potassium,and chloride assays, the reference range for serum sodium is 136-145 mmol/L. [2]

Conditions associated with increased serum sodium (hypernatremia) include the following [3] :

Diverse conditions are associated with decreased serum sodium (hyponatremia); these have been classified in various ways to improve diagnostic accuracy. [4]  One popular classification first advises the exclusion of pseudo-hyponatremic conditions, by checking serum osmolarity first. True hyponatremia is associated with serum hypo-osmolarity. Iso-osmolar “hyponatremia” (hyperlipidemia, paraproteinemia) and hyper-osmolar “hyponatremia” (eg, diabetic ketoacidosis [DKA], mannitol use) may be associated with a normal sodium concentration in the plasma  volume; however, since laboratory values are given for total plasma volume, the presence of other osmotically active particles will lead to the reporting of a lower sodium value. 

True hypo-osmolar (Posm < 275 mEq/L) conditions can be further classified based on volume status and urine sodium excretion [4] :

There are various laboratory methods for the determination of serum/plasma sodium; some have the limitation of the electrolyte exclusion effect, as they measure sodium in the whole sample volume, resulting in falsely low sodium readings in the presence of hyperproteinemia or hyperlipidemia. These methods include flame photometry and indirect ion-selective electrode method (ISE).  Other methods, such as direct ISE, gas electrodes, or freezing-point depression method, measure sodium in the water phase and are thus not subject to the electrolyte exclusion effect. Most clinical chemists have reached the conclusion that direct ISE methods are best; however, two-thirds of laboratories still use the indirect ISE method, and for uniformity of reference values, the direct ISE sodium result is modified (flame mode) to be comparable to the result from indirect ISE. [5]

Specifics for collection and panels are reported for the Architect c System (indirect ion-selective electrode method) as follows [2] :

Related tests are as follows:

Measurement of serum sodium is routine in assessing electrolyte, acid-base, and water balance, as well as renal function. Sodium accounts for approximately 95% of the osmotically active substances in the extracellular compartment, provided that the patient is not in renal failure or does not have severe hyperglycemia. 

The body requires only 1-2 mmol/d of sodium intake, and average daily intake in adults ranges from 90-250 mmol/d. The excess is excreted by the kidneys, which carefully regulate the extracellular sodium level under hormonal influences. Specifically, it is the reabsorption of the last 5-10% of the renally filtered sodium load in the distal tubules via the Na/K and Na/H pumps, under the influence of aldosterone, that primarily affects the amount of sodium excreted in the urine. [5]

Indications for testing of serum sodium/serum electrolytes are as follows:

Drugs that can increase serum sodium include lithium (nephrogenic diabetes insipidus) and (renal impairment).

Drugs that can decrease serum sodium include diuretics (renal loss of sodium) and various iatrogenic causes of SIADH, including cyclophosphamide, carbamazepine, oxcarbazepine, vinca drugs, antipsychotics, and antidepressants. [4]

US Food and Administration. Blood serum chemistry – normal values. Investigations Operations Manual 2015. Available at https://www.fda.gov/downloads/ICECI/Inspections/IOM/UCM135835.pdf.. Accessed: 2018 Sep 7.

Abbott Architect c system manual. [package insert]. Abbott Park, Ill: Abbott Laboratories. 2009.

Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000 May 18. 342 (20):1493-9. [Medline].

Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th ed. New York, NY: McGraw- Hill; 2001.

Rifai N, Horvath AR, Wittwer CT, eds. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. New York, NY: Elsevier; 2018.

Fazia Mir, MD Fellow, Department of Gastroenterology, University of Missouri-Columbia School of Medicine

Fazia Mir, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Ejaz Mahmood, MBBS, MRCGP Resident Physician, Department of Internal Medicine, Einstein Medical Center

Ejaz Mahmood, MBBS, MRCGP is a member of the following medical societies: Philadelphia Endocrine Society

Disclosure: Nothing to disclose.

Catherine Anastasopoulou, MD, PhD, FACE Associate Professor of Medicine, Sidney Kimmel Medical College of Thomas Jefferson University; Attending Endocrinologist, Department of Medicine, Albert Einstein Medical Center

Catherine Anastasopoulou, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Society for Bone and Mineral Research, Endocrine Society, Philadelphia Endocrine Society

Disclosure: Nothing to disclose.

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

Judy Lin, MD

Disclosure: Nothing to disclose.

Serum Sodium 

Research & References of Serum Sodium |A&C Accounting And Tax Services
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