Blood Pressure Reductions With Patiromer Possibly Explained

Evidence suggests decreased sodium absorption could be a contributing factor in at least some patients.
Evidence suggests decreased sodium absorption could be a contributing factor in at least some patients.

CHICAGO—Decreased sodium absorption may explain blood pressure (BP) reductions observed with patiromer treatment for hyperkalemia in patients with low aldosterone levels and low plasma renin activity (PRA), investigators reported at the American Society of Nephrology's 2016 Kidney Week meeting.

BP reductions in patients who do not have low aldosterone levels and low PRA may be due to aldosterone reduction and/or decreased sodium absorption, according to a research team led by Matthew R. Weir, MD, of the University of Maryland School of Medicine in Baltimore.

Patiromer is a novel potassium-binding polymer approved for treating hyperkalemia. It binds potassium in the gastrointestinal tract using calcium rather than sodium ions as the counter-exchange ion to bind potassium. During the 12-week phase 3 OPAL-HK trial, which enrolled 243 patients with chronic kidney disease and hyperkalemia (serum potassium level 5.1 mEq/L or higher), patiromer decreased serum aldosterone concordantly with serum potassium and was associated with decreases in BP, the researchers noted. It is unclear whether BP reductions were due to decreased aldosterone alone, or if reduced sodium absorption with patiromer also contributed to the observed BP effect, they added. To find out, Dr Weir and his collaborators performed a post hoc analysis of the initial treatment phase of OPAL-HK, examining the effect of patiromer on BP in patients with low serum aldosterone and low PRA at baseline. They hypothesized that patiromer treatment would be less likely to decrease BP in patients with lower serum aldosterone at baseline.

The 24 patients who had low aldosterone and low PRA at baseline experienced significant declines in systolic and diastolic BP (-7.8 and -7.6 mm Hg, respectively), similar to the 219 patients who did not have low aldosterone and low PRA at baseline (-5.5 and -3.5, respectively), Dr. Weir's group reported.

At baseline, the low aldosterone/low PRA group had a mean systolic BP of approximately 145 mm Hg and the group without low aldosterone/low PRA had a mean systolic BP of about 140 mm Hg. At week 4 of patiromer treatment, the low aldosterone/low PRA group had a mean systolic BP of approximately 138 mm Hg and the group without low aldosterone/low PRA had mean systolic BP of about 136 mm Hg.

Reference                                                       

  1. Weir MR et al. Aldosterone, renin, and blood pressure during patiromer treatment of hyperkalemia in CKD. Presented in poster format at the 2016 Kidney Week meeting in Chicago, Nov. 15-20.

Disclosure:

The study was supported by Relypsa Inc.

Click here for more coverage from the American Society of Nephrology's Kidney Week 2016 in Chicago.

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