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Evaluate electrolyte balance, acid-base balance; evaluate hypokalemia; Carroll and Oh point out that urinary loss of 40 mmol/24 hours in the presence of hypokalemia <3 mmol/L is excessive.1 In the presence of such hypokalemia, urine excretion is helpful to separate renal from nonrenal losses. Excretion <20 mmol/24 hours is evidence that hypokalemia is not from renal loss.1 Renal loss >50 mmol/L in a hypokalemic, hypertensive patient not on a diuretic may indicate primary or secondary aldosteronism. The kidneys do not respond quickly to potassium deprivation. There is renal wastage of potassium in secondary aldosteronism. Glucocorticoids, including endogenous steroids in Cushing's syndrome, are among the causes of kaliuresis.
Urinary potassium may be elevated with dietary (food and/or medicinal) increase, hyperaldosteronism, renal tubular acidosis, onset of alkalosis, and with other disorders. Time relationships are important in interpretation. Potassium will decrease in Addison's disease and in renal disease with decreased urine flow (nephrosclerosis, pyelonephritis, glomerulonephritis).
