Sorted By Test Name - Mayo Medical Laboratories

RKUR
84475
KCCL
81390
and due to bacterial metabolism of unabsorbed carbohydrates. The fecal water potassium concentration
and daily excretion rate exceeds 3 times normal in association with islet cell tumors and increased
secretion of vasointestinal peptide.
Reference Values:
0-15 years: not established
> or =16 years: 0-199 mEq/kg
Clinical References: 1. Phillips S, Donaldson L, Geisler K: Stool composition in factitial diarrhea: a
6-year experience with stool analysis. Ann Intern Med 1995;123:97-100 2. Agarwal R, Afzalpurkar R,
Fordtran JS: Pathophysiology of potassium absorption and secretion by the human intestine.
Gastroenterology 1994;107:548-571 3. Ho J, Moyer T, Phillips S: Chronic diarrhea: the role of
magnesium. Mayo Clin Proc 1995;70:1091-1092
Potassium, Random, Urine
Clinical Information: Potassium (K+) is the major intracellular cation. Functions of K+ include
regulation of neuromuscular excitability, heart contractility, intracellular fluid volume, and hydrogen ion
concentration. The physiologic function of K+ requires that the body maintain a low extracellular fluid
(ECF) concentration of the cation; the intracellular K+ concentration is 20 times greater than the
extracellular concentration. Only 2% of total body K+ circulates in the plasma. The kidneys provide the
most important regulation of K+. The proximal tubules reabsorb almost all the filtered K+. Under the
influence of aldosterone, the remaining K+ can then be secreted into the urine in exchange for sodium in
both the collecting ducts and the distal tubules. Thus, the distal nephron is the principal determinant of
urinary K+ excretion. Decreased excretion of K+ in acute renal disease and end-stage renal failure are
common causes of prolonged hyperkalemia. Renal losses of K+ may occur during the diuretic (recovery)
phase of acute tubular necrosis, during administration of nonpotassium sparing diuretic therapy, and
during states of excess mineralo- corticoid or glucocorticoid.
Useful For: Determining the cause for hyper- or hypokalemia
Interpretation: Hypokalemia reflecting true total body deficits of K+ can be classified into renal and
nonrenal losses based on the daily excretion of K+ in the urine. During hypokalemia, if urine excretion of
K+ is 30 mEq/d in a hypokalemia setting is inappropriate and indicates that the kidneys are the
primary source of the lost K+.
Reference Values:
No established reference values
Clinical References: 1. Tietz Textbook of Clinical Chemistry. 3rd edition. Edited by CA Burtis, ER
Ashwood. Philadelphia, WB Saunders Co, 2001 2. Toffaletti J: Electrolytes. In Professional Practice in
Clinical Chemistry: A Review. Edited by DR Dufour, N Rifai. Washington, AACC Press, 1993
Potassium, Serum
Clinical Information: Potassium (K) is the major cation of the intracellular fluid. Disturbance of
potassium homeostasis has serious consequences. Decreases in extracellular potassium are characterized
by muscle weakness, irritability, and eventual paralysis. Cardiac effects include tachycardia, other cardiac
conduction abnormalities that are apparent by electrocardiographic examination, and eventual cardiac
arrest. Hypokalemia (low K) is common in vomiting, diarrhea, alcoholism, and folic acid deficiency.
Additionally, >90% of hypertensive patients with aldosteronism have hypokalemia. Abnormally high
extracellular K levels produce symptoms of mental confusion; weakness, numbness and tingling of the
extremities; weakness of the respiratory muscles; flaccid paralysis of the extremities; slowed heart rate;
and eventually peripheral vascular collapse and cardiac arrest. Hyperkalemia may be seen in end-stage
renal failure, hemolysis, trauma, Addison's disease, metabolic acidosis, acute starvation, dehydration, and
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