|Values are valid only on day of printing.|
Assessing acid-base balance, water balance, water intoxication, and dehydration
Sodium (Na+) is the primary extracellular cation. Na+ 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 to 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. Na+ is freely filtered by the glomeruli. Approximately 70% to 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% to 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% to 10% of the filtered load. It is the regulation of this latter fraction of filtered Na+ that determines the amount of Na+ excreted in the urine.
No established reference values
Urinary sodium (Na+) excretion varies with dietary intake, and there is a large diurnal variation with the rate of Na+ excretion during the night being only 20% of the peak rate during the day.
Na+ may be lost in the kidneys as a result of diuretic therapy, salt-losing nephropathies, or adrenal insufficiency, with the urinary Na+ concentration usually more than 20 mEq/L. In these hypovolemic states, urine Na+ values <10 mEq/L indicate extrarenal Na+ loss. In hypervolemic states, a low urine Na+ (<10 mEq/L) may indicate nephrotic syndrome in addition to nonrenal causes.
No significant cautionary statements
Tietz Textbook of Clinical Chemistry. Third edition. Edited by CA Burtis, ER Ashwood. Philadelphia, WB Saunders Company, 2001