This patient has widespread destruction of both adrenal glands, which means that she will lose both her mineralocorticoids and her glucocorticoids. The loss of the mineralocorticoids and the effect on the kidneys is what is being tested here. When aldosterone is functioning and abundant, it has several critical functions on the nephron. First, it upregulates Na+/K+ ATPase expression on the basolateral membrane, establishing a strong electrochemical gradient that better absorbs Na+, while the increased intracellular K+ concentration makes it easier to lose K+ from the cell into the lumen. Aldosterone also upregulates the expression of epithelial sodium channels (ENaC) on the collecting duct, reabsorbing more Na+. Finally, aldosterone increases expression of H+ ATPases on alpha-intercalated cells of the collecting duct, which are responsible for secreting H+ (this is part of contraction alkalosis).

With the loss of aldosterone, we will see a decreases Na+/K+ gradient and decreased Na+ reabsorption; this leads to decreased serum sodium and increased serum potassium. At the same time, not expressing H+ ATPases will lead to H+ not being secreted, creating a more acidic environment (pH will decrease).