IN 1957 Hudson et al.1 described a patient with isolated hypoaldosteronism who had hyperkalemia with low urinary aldosterone excretion, normal glucocorticoid secretion, and relatively normal renal function. We have since recognized a variety of disorders associated with decreased aldosterone secretion and action, and other disorders that mimic them. The principal action of aldosterone is to stimulate renal sodium reabsorption and potassium excretion. It acts as a permease at the luminal membrane of distal renal tubular cells to facilitate the entry of sodium into these cells. It also stimulates the activity of Na+/K+-transporting ATPase in the basolateral membrane, which.
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