Potassium Binding for Conservative and Preservative Management of Chronic Kidney Disease

Deborah J. Clegg; Biff F. Palmer


Curr Opin Nephrol Hypertens. 2020;29(1):29-38. 

In This Article


Patiromer is a K+-binding agent approved for the treatment of hyperkalemia. The drug is a nonabsorbed polymer, which binds K+ in exchange for Ca2+ in the gastrointestinal tract, predominately in the colon.[30] Like SPS, patiromer is nonselective and may also bind Mg2+ and a small amount of Na+. Patiromer has an onset of action of 7 h and is typically given at a dose of 8.4 g once daily[31] (Table 2). When used as maintenance therapy, it is recommended that the dose of patiromer be increased in 8.4-g increments at at least 1-week intervals.

The efficacy and safety of patiromer in patients with CKD and/or heart failure receiving RAASi blockers has been established in several key clinical studies described in Table 3.[32–34] In these studies, patiromer significantly reduced serum K+ concentrations and facilitated continuation and up titration of RAASi therapy. For example, in the PEARL-HF study significantly more patients treated with patiromer were able to increase their spironolactone dose from 25 to 50 mg/day versus those receiving placebo (91 vs. 74%; P = 0.019) without experiencing hyperkalemia.[34] In the OPAL-HK study, 94% of patients in the patiromer group were able to continue RAASi therapy, whereas discontinuation of these drugs was required in 56% of patients receiving placebo because of recurrence of hyperkalemia.[32] In the AMETHYST-DN study, serum K+ concentrations were reduced with patiromer through week 4 of treatment, and K+ was maintained in a normal range over 52 weeks demonstrating the durability of this treatment approach.[33] The use of patiromer to facilitate use of spironolactone in CKD patients with resistant hypertension was tested in the AMBER trial.[35] In this multicenter, double-blind, placebo-controlled randomized trial of 295 patients with CKD (eGFR between 25 and 45 ml/min/1.73 m2) and resistant hypertension, patients were randomized to either spironolactone with placebo or spironolactone and patiromer. Although change in SBP between groups was similar, use of spironolactone was associated with an 11–12 mmHg reduction overall. At week 12, 66% of patients in the placebo group remained on spironolactone compared with 86% of patients in the patiromer group. Patients treated with patiromer were able to use 385 mg more of spironolactone during this time. Finally, while two out of three patients treated with placebo developed hyperkalemia, patiromer reduced this risk by half.