Significant hyperkalemia and hyponatremia secondary to telmisartan/hydrochlorothiazide treatment.

The renin-angiotensin-aldosterone system (RAAS) has crucial importance in maintaining blood pressure; thus blockade of RAAS is an effective antihypertensive treatment choice. The final step in RAAS stimulation is aldosterone secretion by angiotensin II, which leads to increased renal tubular sodium absorption and potassium secretion. Angiotensin II receptor blockers (ARBs) allow blockade of RAAS by blocking binding of angiotensin II to the AT(1) receptors. There are several fixed-dose combinations of ARBs with hydrochlorothiazide in the market, providing antihypertensive therapies with complimentary mechanisms of action. With such combinations, while ARB inhibits the vasoconstricting action and aldosterone-secreting effects of angiotensin II, hydrochlorothiazide affects the renal tubular mechanisms of electrolyte reabsorption and directly increases excretion of sodium and chloride in the distal tubule, and promotes water excretion. Also, hypokalemia, which may be triggered by increased urinary potassium loss induced by hydrochlorothiazide, is opposed by ARB use and hence ARB/hydrochlorothiazide combination is known to be safe in terms of potassium imbalance. In this case report, significant hyperkalemia and hyponatremia related to telmisartan/hydrochlorothiazide use in a diabetic patient has been presented.