Urinary excretion of potassium is increased in primary aldosteronism. It is often increased in dehydration and in salicylate toxicity. Decreased levels are seen in malabsorption.
(Specimen Container)
24-hour urine container
(Transport Temperature)
Temperature | Period |
---|---|
Room temperature | 14 days |
Refrigerated | 14 days |
Frozen | 30 days |
10 mL aliquot of a 24-hour urine collected in a no preservative plastic urine container . Record total volume and collection duration on specimen container and test requisition
Potassium (K+) is the major intracellular cation. Functions of potassium 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 concentration is 20 times greater than the extracellular K+ 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.
22 – 160 mmol/24 hr