||The answer is A.
This man’s electrolyte pattern is consistent with a hyporeninemic hypoaldosteronism state, or type IV renal tubular acidosis.
The defect is believed to be due to an insufficiency of both angiotensin- and adrenal mineralocorticoid-secreting capacity. Inhibition of the renin-angiotensin system by beta-adrenergic blockade such as propranolol can cause hyperkalemia;
in addition, nonsteroidal anti-inflammatory agents or angiotensin-converting enzyme (ACE)
inhibitors may also lead to hyperkalemia.
The use of carbenicillin, theophyllin, and hydrochlorothiazide promote the loss of potassium through the distal renal tubule.
Calcium channel blockers such as verapamil have no significant effect on serum potassium concentrations at the usual doses.