A 56-year-old man with type 2 diabetes mellitus, hypertension, and chronic kidney disease is found to have a persistently elevated serum potassium level. He takes lisinopril. Blood pressure is 130/90 mm Hg. Physical examination shows no abnormalities. The patient is prescribed patiromer therapy. Which of the following best describes the mechanism of action of this medication?

Question

A 56-year-old man with type 2 diabetes mellitus, hypertension, and chronic kidney disease is found to have a persistently elevated serum potassium level.  He takes lisinopril.  Blood pressure is 130/90 mm Hg.  Physical examination shows no abnormalities.  The patient is prescribed patiromer therapy.  Which of the following best describes the mechanism of action of this medication?

Quizplus · Accepted Answer

11ec160b_3c6d_e897_9249_d312c7310466_MD0001_00 Hyperkalemia is a common complication of chronic kidney disease that results from impaired potassium excretion. Medications that inhibit the renin-angiotensin-aldosterone system (eg, ACE inhibitors, mineralocorticoid blockers) can also worsen hyperkalemia, often limiting their use in this population. Patiromer is a nonabsorbable cation exchange resin that binds colonic potassium in exchange for calcium, trapping potassium within the resin where it is then excreted in the feces. It is often used for treatment of chronic hyperkalemia. However, onset of action takes several hours, so it is not recommended as monotherapy in acute hyperkalemia. Adverse effects include gastrointestinal disturbance (eg, diarrhea), hypokalemia, hypercalcemia (due to luminal exchange of calcium), and hypomagnesemia (due to off-target binding of other positive ions). Patiromer may also bind certain medications (eg, ciprofloxacin, levothyroxine). Sodium zirconium cyclosilicate is another nonabsorbable cation exchange resin that binds intestinal potassium in exchange for sodium and hydrogen. It is more selective for potassium and does not interfere with absorption of magnesium or other medications. However, the increased sodium load may be problematic for patients sensitive to exogenous sodium (eg, cirrhosis, congestive heart failure). (Choice A) Beta-2 agonists and insulin increase the activity of the Na⁺-K⁺-ATPase in skeletal muscles, which transiently increases intracellular translocation of potassium. These medications are used in the treatment of acute, severe hyperkalemia but do not have a sustained potassium-lowering effect. (Choice B) Mineralocorticoid blockers (eg, spironolactone, eplerenone) antagonize the effects of aldosterone in the renal tubules. This leads to increased reabsorption of potassium, which will worsen hyperkalemia. (Choice C) Calcium gluconate antagonizes the effects of hyperkalemia on cell membrane potential and is used in severe hyperkalemia to stabilize cardiac myocytes and prevent arrhythmias. It does not lower serum potassium levels. (Choice E) Loop diuretics (eg, furosemide) increase renal excretion of potassium. Patiromer inhibits dietary potassium absorption and therefore decreases the total amount of renally excreted potassium. Educational objective: Patiromer is a nonabsorbable cation exchange resin used to treat hyperkalemia. It binds colonic potassium in exchange for calcium, trapping potassium within the resin where it is then excreted in the feces. Adverse effects include diarrhea, hypokalemia, hypercalcemia, and hypomagnesemia.

A 56-Year-Old Man with Type 2 Diabetes Mellitus, Hypertension, and Chronic