Sorted By Test Name - Mayo Medical Laboratories

NACCL
81692
NAU
8525
Clinical References: Tietz Textbook of Clinical Chemistry. 3rd edition. Edited by CA Burtis, ER
Ashwood. Philadelphia, WB Saunders Co., 2001
Sodium, Serum
Clinical Information: 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. Hypoatremia (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 (e.g., 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 (i.e., 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.
Useful For: Sodium assays are important in assessing acid-base balance, water balance, water
intoxication, and dehydration.
Interpretation: Symptoms of hyponatremia depend primarily upon the rate of change in sodium
concentration, rather than the absolute level. Typically, sodium values less than 120 mEq/L result in
weakness; values less than 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.
Reference Values:
> or =12 months: 135-145 mmol/L
Reference values have not been established for patients that are less than 12 months of age.
Clinical References: Tietz Textbook of Clinical Chemistry, Edited by Burtis and Ashwood. WB
Saunders Co, Philadelphia, PA, 1994
Sodium, Urine
Clinical Information: Sodium (Na+) 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
Na+in the body is a reflection of the balance between Na+ intake and output. The normal daily diet
contains 8 to 15 grams of sodium chloride (NaCl) which is nearly completely absorbed from the
gastrointestinal tract. The body requires only 1-2 mmol/d, and the excess is excreted by the kidneys,
which are the ultimate regulators of the amount of Na+ (and thus water) in the body. Sodium is freely
filtered by the glomeruli. Approximately 70-80% of the filtered Na+ is actively reabsorbed in the
proximal tubules with chloride and water passively following in an iso-osmotic and electrically neutral
manner. Another 20-25% is reabsorbed in the loop of Henle along with chloride and more water. In the
distal tubules, interaction of the adrenocortical hormone aldosterone with the coupled sodium-potassium
and sodium- hydrogen exchange systems directly results in the reabsorption of Na+ and indirectly of
chloride from the remaining 5-10% of the filtered load. It is the regulation of this latter fraction of filtered
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