The potassium regulator patiromer affects serum and stool electrolytes in patients receiving hemodialysis

Abstract

Hyperkalemia is a common and an important cause of death in maintenance hemodialysis patients. Here we investigated the effect of patiromer, a synthetic cation exchanger, to regulate potassium homeostasis. Serum and stool electrolytes were measured in 27 anuric patients with hyperkalemia receiving hemodialysis (mainly 2 mEq/L dialysate) during consecutive two weeks of no-treatment, 12 weeks of treatment with patiromer (16.8g once daily), and six weeks of no treatment. The serum potassium decreased from a mean of 5.7 mEq/L pre-treatment to 5.1 mEq/L during treatment and rebounded to 5.4 mEq/L post-treatment. During the treatment phase, serum calcium significantly increased (from 8.9 to 9.1 mg/dL) and serum magnesium significantly decreased (from 2.6 to 2.4 mg/dL) compared to pre-treatment levels. For each one mEg/L increase in serum magnesium, serum potassium increased by 1.07 mEq/L. Stool potassium significantly increased during treatment phase from pre-treatment levels (4132 to 5923 μg/g) and significantly decreased post-treatment to 4246 μg/g. For each one μg/g increase in stool potassium, serum potassium significantly declined by 0.05 mEq/L. Stool calcium was significantly higher during the treatment phase (13017 μg/g) compared to pre-treatment (7874 μg/g) and post-treatment (7635 μg/g) phases. We estimated that 16.8 g of patiromer will increase fecal potassium by 1880 μg/g and reduce serum potassium by 0.5 mEq/L. Thus, there is a complex interaction between stool and blood potassium, calcium and magnesium during patiromer treatment. Long term consequence of patiromer-induced changes in serum calcium and magnesium remains to be studied.

Keywords: calcium; hyperkalemia; magnesium; phosphate; potassium binder; sodium.