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Assessing acid-base balance, water balance, water intoxication, and dehydration
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 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. Sodium 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.
41-227 mmol/24 hours
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.
Sodium 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 non-renal causes.
No significant cautionary statements
Tietz Textbook of Clinical Chemistry. Third edition. Edited by CA Burtis, ER Ashwood. Philadelphia, WB Saunders Company, 2001