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Sorted By Test Name - Mayo Medical Laboratories

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RNAUR<br />

84522<br />

+ potassium) unless there are exogenous factors inducing a change in this ratio, such as the presence of<br />

other osmotic agents (magnesium sulfate, saccharides), or drugs inducing secretions, such as<br />

phenolphthalein or bisacodyl. If the relationship between osmolality, potassium, and sodium (see equation<br />

above) indicates an osmotic gap, diarrhea may be osmotically induced by exogenous agents such as<br />

magnesium sulfate or saccharides. If there is no osmotic gap but sodium concentration is 2 to 3 times<br />

normal, secretory diarrhea may be the cause, and agents such as phenolphthalein, bisacodyl, or cholera<br />

toxin should be suspected.<br />

Useful For: Determining the cause of chronic diarrhea<br />

Interpretation: Typically, stool sodium is similar to serum since the gastrointestinal (GI) tract does<br />

not secrete water. A useful formula is 2x (stool sodium + stool potassium) = stool osmolality + or - 30<br />

mOsm. Increased fecal sodium content or daily excretion rate with normal fecal potassium and no osmotic<br />

gap indicates secretory diarrhea. Normal fecal sodium and potassium in the presence of an osmotic gap<br />

(>30 mOsm/kg) suggests osmotic diarrhea. Normal or low fecal sodium in association with high fecal<br />

potassium suggests deterioration of the epithelial membrane or a bleeding lesion. High sodium and<br />

potassium in the absence of an osmotic gap indicate active electrolyte transport in the GI tract that might<br />

be induced by agents such as cholera toxin or hypersecretion of vasointestinal peptide. If sodium<br />

concentration or 24-hour sodium excretion rate is 2 to 3 times normal and osmotic gap >30 mOsm/kg,<br />

secretory diarrhea may be the cause. Agents such as phenolphthalein, bisacodyl, or cholera toxin should<br />

be suspected. For very low stool osmolality, consider factitial diarrhea.<br />

Reference Values:<br />

0-15 years: not established<br />

> or =16 years: 0-159 mEq/kg<br />

Clinical References: 1. Phillips S, Donaldson L, Geisler K, et al: Stool composition in factitial<br />

diarrhea: a 6-year experience with stool analysis. Ann Intern Med 1995;123:97-100 2. Ho J, Moyer T,<br />

Phillips S: Chronic diarrhea: the role of magnesium. <strong>Mayo</strong> Clin Proc 1995;70:1091-1092<br />

Sodium, Random, Urine<br />

Clinical Information: Sodium (Na+) is the primary extracellular cation. Na+ is responsible for<br />

almost one half the osmolality of the plasma and, therefore, plays a central role in maintaining the normal<br />

distribution of water and the osmotic pressure in the extracellular fluid compartment. The amount of Na+<br />

in the body is a reflection of the balance between Na+ intake and output. The normal daily diet contains 8<br />

to 15 grams of sodium chloride (NaCl), which is nearly completely absorbed from the gastrointestinal<br />

tract. The body requires only 1 to 2 mmol/d, and the excess is excreted by the kidneys, which are the<br />

ultimate regulators of the amount of Na+ (and thus water) in the body. Na+ is freely filtered by the<br />

glomeruli. Approximately 70-80% of the filtered Na+ is actively reabsorbed in the proximal tubules with<br />

chloride and water passively following in an iso-osmotic and electrically neutral manner. Another 20% to<br />

25% is reabsorbed in the loop of Henle along with chloride and more water. In the distal tubules,<br />

interaction of the adrenocortical hormone aldosterone with the coupled sodium-potassium and sodiumhydrogen<br />

exchange systems directly results in the reabsorption of Na+ and indirectly of chloride from the<br />

remaining 5% to 10% of the filtered load. It is the regulation of this latter fraction of filtered Na+ that<br />

determines the amount of Na+ excreted in the urine.<br />

Useful For: Assessing acid-base balance, water balance, water intoxication, and dehydration<br />

Interpretation: Urinary Na+ excretion varies with dietary intake, and there is a large diurnal variation<br />

with the rate of Na+ excretion during the night being only 20% of the peak rate during the day. Na+ may<br />

be lost in the kidneys as a result of diuretic therapy, salt-losing nephropathies, or adrenal insufficiency,<br />

with the urinary Na+ concentration usually more than 20 mEq/L. In these hypovolemic states, urine Na+<br />

values

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