NACCL - Clinical: Sodium, Serum

Test Catalog

Test Name

Test ID: NACCL    
Sodium, Serum

Useful For Suggests clinical disorders or settings where the test may be helpful

Sodium assays are important in assessing acid-base balance, water balance, water intoxication, and dehydration.

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Sodium is the primary extracellular cation. Sodium is responsible for almost one half the osmolality of the plasma and therefore plays a central role in maintaining the normal distribution of water and the osmotic pressure in the extracellular fluid compartment. The amount of sodium in the body is a reflection of the balance between sodium intake and output.


Hyponatremia (low sodium) is a predictable consequence of decreased intake of sodium, particularly that precipitated or complicated by unusual losses of sodium from the gastrointestinal tract (eg, vomiting and diarrhea), kidneys or sweat glands. Renal loss may be caused by inappropriate choice, dose or use of diuretics; by primary or secondary deficiency of aldosterone and other mineralocorticoids; or by severe polyuria. It is common in metabolic acidosis. Hyponatremia also occurs in nephrotic syndrome, hypoproteinemia, primary and secondary adrenocortical insufficiency and congestive heart failure. Symptoms of hyponatremia are a result of brain swelling and range from weakness to seizures, coma and death.


Hypernatremia (high sodium) is often attributable to excessive loss of sodium-poor body fluids. Hypernatremia is often associated with hypercalcemia and hypokalemia and is seen in liver disease, cardiac failure, pregnancy, burns, and osmotic diuresis. Other causes include decreased production of ADH or decreased tubular sensitivity to the hormone (ie, diabetes insipidus), inappropriate forms of parenteral therapy with saline solutions, or high salt intake without corresponding intake of water. Hypernatremia occurs in dehydration, increased renal sodium conservation in hyperaldosternism, Cushing's syndrome, and diabetic acidosis. Severe hypernatremia may be associated with volume contraction, lactic acidosis and increased hematocrit. Symptoms of hypernatremia range from thirst to confusion, irritability, seizures, coma and death.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

> or =12 months: 135-145 mmol/L

Reference values have not been established for patients that are less than 12 months of age.

Interpretation Provides information to assist in interpretation of the test results

Symptoms of hyponatremia depend primarily upon the rate of change in sodium concentration, rather than the absolute level. Typically, sodium values <120 mEq/L result in weakness; values <100 mEq/L in bulbar or pseudobulbar palsy; and values between 90 and 105 mEq/L in severe signs and symptoms of neurological impairment.


Symptoms associated with hypernatremia depend upon the degree of hyperosmolality present.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

It is important to remember that whole blood sodium values determined by direct potentiometry-ion selective electrode will be higher in specimens with high protein and lipid concentrations than the corresponding serum specimen that is assayed by an indirect potentiometric method. The whole blood sodium values are the correct values.


Ion selective electrodes are selective but not absolutely specific for the ion in question. Other monovalent cations may react with the electrode but not in the physiologic range.

Clinical Reference Recommendations for in-depth reading of a clinical nature

Tietz Textbook of Clinical Chemistry. Edited by CA Burtis, ER Ashwood. WB Saunders Company. Philadelphia, PA, 1994