Renin-angiotensin-aldosterone system inhibitors (RAASis) are beneficial and recommended for patients with chronic kidney disease (CKD) and type 2 diabetes mellitus (T2DM) [ADA. Diabetes Care. 2014]. However, hyperkalemia (HK) often limits RAASi therapy [Einhorn LM et al. Arch Intern Med. 2009]. Current treatment options for chronic management of HK are limited [Fordjour KN et al. Am J Med Sci. 2014; Harel Z et al. Am J Med. 2013], and an unmet need remains for safe and effective HK treatment.

Patiromer has previously been shown to normalize serum potassium (s-K⁺) and prevent HK recurrence compared with placebo in A Two-Part, Single-Blind, Phase 3 Study Evaluating the Efficacy and Safety of Patiromer for the Treatment of Hyperkalemia [OPAL-HK; NCT01810939]. Matthew R. Weir, MD, University of Maryland, Baltimore, Maryland, USA, presented poster FR-PO792, which described the prespecified analysis of the subgroup with T2DM in OPAL-HK.

In part A (4-week treatment phase), patients with CKD with and without T2DM on stable doses of ≥ 1 RAASi with mild HK (s-K⁺ 5.1 to < 5.5 mEq/L; n = 92) received patiromer 4.2 g BID; those with moderate-to-severe HK (s-K⁺ 5.5 to < 6.5 mEq/L; n = 151) received patiromer 8.4 g BID. After 4 weeks, patients with moderate-to-severe HK continued on to the 8-week withdrawal phase (part B) and were randomly assigned to patiromer plus RAASi (n = 55) or placebo plus RAASi (n = 52).

End points included change in s-K⁺ from baseline to week 4, percentage of patients with s-K⁺ within target at week 4, between-group difference in s-K⁺ change over the first 4 weeks, and percentage of patients with recurrent HK.

T2DM was present in 138 (57%) of patients assessed for the primary end point. The mean change from baseline to week 4 for patients with T2DM was −1.00 ± 0.04 (95% CI, −1.08 to −0.92; P < .001); for those without T2DM it was −1.02 ± 0.05 (95% CI, −1.12 to −0.92; P < .001); (P = .77 for interaction). In a secondary end point, 78% and 73% of patients with and without T2DM, respectively, had s-K⁺ within range at week 4.

The median increase in s-K⁺ from baseline at week 4 of the withdrawal phase was larger for the placebo group (n = 33; 0.69 mEq/L; 95% CI, 0.19 to 1.29) than for the patiromer group (n = 34; 0.03 mEq/L; 95% CI, −0.20 to 0.30; P < .001) in patients with T2DM (P < .001).

Patiromer increased the time to first recurrent HK event vs placebo in patients with T2DM. Through week 8 of the withdrawal phase, significantly (P < .001) more T2DM patients on placebo (62%) vs patiromer (19%) had at least 1 recurrent HK event.

Patiromer was well tolerated in patients with T2DM, with mild-to-moderate constipation being the most common adverse event (13% in Part A, 6% in Part B).

For patients with CKD, T2DM, and HK who are taking RAASis, patiromer may provide an option for HK management.