A 45-year-old man comes to the office for routine follow-up. The patient was diagnosed with hypertension and hypercholesterolemia a year ago and is taking hydrochlorothiazide and amiloride daily. He currently feels well. He does not use tobacco, alcohol, or illicit drugs. Blood pressure is 135/85 mm Hg. Physical examination is unremarkable. Laboratory results are as follows: There was no evidence of hemolysis when the blood sample was checked by the laboratory technician. ECG demonstrates normal sinus rhythm with no other abnormalities. Which of the following is the most appropriate next step in management of this patient?

Question

A 45-year-old man comes to the office for routine follow-up.  The patient was diagnosed with hypertension and hypercholesterolemia a year ago and is taking hydrochlorothiazide and amiloride daily.  He currently feels well.  He does not use tobacco, alcohol, or illicit drugs.  Blood pressure is 135/85 mm Hg.  Physical examination is unremarkable.  Laboratory results are as follows:  There was no evidence of hemolysis when the blood sample was checked by the laboratory technician.  ECG demonstrates normal sinus rhythm with no other abnormalities.  Which of the following is the most appropriate next step in management of this patient?

Quizplus · Accepted Answer

11ec25c8_d4e1_fe68_bc81_83b66100bb46_MD0003_00 This patient's hyperkalemia is likely due to amiloride, a potassium-sparing diuretic that blocks the epithelial sodium channel (ENaC) in the renal collecting system. Sodium normally enters the apical end of the principal cell in the renal collecting system through the ENaC and is subsequently pumped out of the basolateral end through the 3Na⁺/2K⁺-ATPase. This creates an electronegative environment in the collecting tubule, which generates a gradient for potassium to leave the intracellular space and enter the urine for excretion. Blockade of the ENaC by amiloride limits the electronegative charge in the collecting system lumen, thereby reducing potassium excretion; the result is hyperkalemia in a minority of patients. Some individuals also develop metabolic acidosis due to a reduced gradient for hydrogen cation excretion. renal collecting system Because hyperkalemia can result in life-threatening cardiac arrhythmia, patients who develop hyperkalemia while taking potassium-sparing diuretics should discontinue the medication and start a new antihypertensive agent (eg, amlodipine). Asymptomatic individuals with mild or moderate elevations in potassium (eg, <6.5 mEq/L) do not require urgent treatment (eg, calcium gluconate, insulin plus dextrose); however, potassium level should be rechecked in 1-2 weeks to ensure improvement. (Choice B) Hydrochlorothiazide blocks the apical sodium-chloride channel in the distal convoluted tubule; this increases sodium delivery to the collecting tubules, which promotes potassium excretion (ie, more sodium is absorbed, creating a stronger gradient for potassium excretion). Therefore, thiazides can cause hypokalemia, not hyperkalemia. (Choices C and D) Intravenous calcium counters the effect of hyperkalemia on the cell membrane, and insulin plus glucose drives potassium into cells due to increased activity of the Na+/K+-ATPase. These drugs temporarily reverse life-threatening effects of hyperkalemia and are used to treat hyperkalemic emergency (eg, arrhythmia, ECG changes); patients with mild or moderate hyperkalemia do not require urgent treatment but should have close follow-up. (Choice E) Increased dietary potassium intake can cause hyperkalemia in patients with hypoaldosteronism or kidney disease. However, it is not a significant cause of hyperkalemia in patients with normal kidney function. A low-potassium diet is not likely to have a significant effect on this patient but may be used as part of subacute treatment in some patients. Educational objective: Potassium-sparing diuretics (eg, amiloride) can cause hyperkalemia due to inhibition of the epithelial sodium channel in the renal collecting tubule. Patients with asymptomatic mild or moderate hyperkalemia (eg, potassium level <6.5 mEq/L) can usually be managed with medication or dietary changes. Those with severe manifestations of hyperkalemia require urgent therapy (eg, calcium gluconate, insulin plus dextrose). References: Management of hyperkalemia. (http://www.ncbi.nlm.nih.gov/pubmed/24087806) Hyperkalemia. (http://www.ncbi.nlm.nih.gov/pubmed/16445274)

A 45-Year-Old Man Comes to the Office for Routine Follow-Up