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Mayo Test Catalog, (Sorted By Test Name) - Mayo Medical ...

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RKUR<br />

84475<br />

carbohydrates passing through the GI tract.<br />

Useful For: Work-up of a patient with chronic diarrhea<br />

Interpretation: Typically, stool potassium is 20 times serum potassium. A useful formula is 2x (stool<br />

sodium + stool potassium) = stool osmolality + or - 30 mOsm. Fecal potassium concentration and daily<br />

excretion rate are usually below the median level in patients with osmotic diarrhea. Normal fecal sodium<br />

and potassium in the presence of an osmotic gap (>30 mOsm/kg) suggests osmotic diarrhea. Increased<br />

fecal sodium content or daily excretion rate with normal fecal potassium and no osmotic gap indicates<br />

secretory diarrhea. High fecal potassium in association with normal or low fecal sodium suggests<br />

deterioration of the epithelial membrane or a bleeding lesion. High sodium and potassium (3 times<br />

normal) in the absence of an osmotic gap indicate active electrolyte transport in the gastrointestinal (GI)<br />

tract that might be induced by agents such as cholera toxin, hypersecretion of vasointestinal peptide, or<br />

islet cell tumor. For very low stool osmolality, consider factitial diarrhea. The fecal potassium<br />

concentration and excretion rate are increased 2-fold to 3-fold with ulcerative colitis, or bleeding into the<br />

GI tract, when exposed to cholera toxin, with ingestion of mineralocorticoids, in primary aldosteronism,<br />

and due to bacterial metabolism of unabsorbed carbohydrates. The fecal water potassium concentration<br />

and daily excretion rate exceeds 3 times normal in association with islet cell tumors and increased<br />

secretion of vasointestinal peptide.<br />

Reference Values:<br />

0-15 years: not established<br />

> or =16 years: 0-199 mEq/kg<br />

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

6-year experience with stool analysis. Ann Intern Med 1995;123:97-100 2. Agarwal R, Afzalpurkar R,<br />

Fordtran JS: Pathophysiology of potassium absorption and secretion by the human intestine.<br />

Gastroenterology 1994;107:548-571 3. Ho J, Moyer T, Phillips S: Chronic diarrhea: the role of<br />

magnesium. <strong>Mayo</strong> Clin Proc 1995;70:1091-1092<br />

Potassium, Random, Urine<br />

Clinical Information: Potassium (K+) is the major intracellular cation. Functions of K+ include<br />

regulation of neuromuscular excitability, heart contractility, intracellular fluid volume, and hydrogen ion<br />

concentration. The physiologic function of K+ requires that the body maintain a low extracellular fluid<br />

(ECF) concentration of the cation; the intracellular K+ concentration is 20 times greater than the<br />

extracellular concentration. Only 2% of total body K+ circulates in the plasma. The kidneys provide the<br />

most important regulation of K+. The proximal tubules reabsorb almost all the filtered K+. Under the<br />

influence of aldosterone, the remaining K+ can then be secreted into the urine in exchange for sodium in<br />

both the collecting ducts and the distal tubules. Thus, the distal nephron is the principal determinant of<br />

urinary K+ excretion. Decreased excretion of K+ in acute renal disease and end-stage renal failure are<br />

common causes of prolonged hyperkalemia. Renal losses of K+ may occur during the diuretic (recovery)<br />

phase of acute tubular necrosis, during administration of nonpotassium sparing diuretic therapy, and<br />

during states of excess mineralo- corticoid or glucocorticoid.<br />

Useful For: Determining the cause for hyper- or hypokalemia<br />

Interpretation: Hypokalemia reflecting true total body deficits of K+ can be classified into renal and<br />

nonrenal losses based on the daily excretion of K+ in the urine. During hypokalemia, if urine excretion of<br />

K+ is 30 mEq/d in a hypokalemia setting is inappropriate and indicates that the kidneys are the<br />

primary source of the lost K+.<br />

Reference Values:<br />

No established reference values<br />

Clinical References: 1. Tietz Textbook of Clinical Chemistry. 3rd edition. Edited by CA Burtis, ER<br />

Ashwood. Philadelphia, WB Saunders Co, 2001 2. Toffaletti J: Electrolytes. In Professional Practice in<br />

Current as of January 3, 2013 2:22 pm CST 800-533-1710 or 507-266-5700 or <strong>Mayo</strong><strong>Medical</strong>Laboratories.com Page 1466

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