Treatment with patiromer decreases aldosterone in patients with chronic kidney disease and hyperkalemia on renin-angiotensin system inhibitors

Elevated serum aldosterone can be vasculotoxic and facilitate cardiorenal damage. Renin-angiotensin system inhibitors reduce serum aldosterone levels and/or block its effects but can cause hyperkalemia. Patiromer, a nonabsorbed potassium binder, decreases serum potassium in patients with chronic kidney disease on renin-angiotensin system inhibitors. Here we examined the effect of patiromer treatment on serum aldosterone, blood pressure, and albuminuria in patients with chronic kidney disease on renin-angiotensin system inhibitors with hyperkalemia (serum potassium 5.1-6.5 mEq/l). We analyzed data from the phase 3 OPAL-HK study (4-week initial treatment phase of 243 patients; 8-week randomized withdrawal phase of 107 patients). In the treatment phase, the (mean +/- standard error) serum potassium was decreased concordantly with the serum aldosterone (-1.99 +/- 0.51 ng/dl), systolic/diastolic blood pressure (-5.64 +/- 1.04 mm Hg/ -3.84 +/- 0.69 mm Hg), and albumin-to-creatinine ratio (-203.7 +/- 54.7 mg/g), all in a statistically significant manner. The change in the plasma renin activity (-0.44 +/- 0.63 mu g/l/hr) was not significant. In the withdrawal phase, mean aldosterone levels were sustained with patiromer (+0.23 +/- 1.07 ng/dl) and significantly increased with placebo (+2.78 +/- 1.25 ng/dl). Patients on patiromer had significant reductions in mean systolic/diastolic blood pressure (-6.70 +/- 1.59/-2.15 +/- 1.06 mm Hg), whereas those on placebo did not (-1.21 +/- 1.89 mm Hg/+ 1.72 +/- 1.26 mm Hg). Significant changes in plasma renin activity were found only in the placebo group (-3.90 +/- 1.41 mu g/l/hr). Thus, patiromer reduced serum potassium and aldosterone levels independent of plasma renin activity in patients with chronic kidney disease and hyperkalemia on renin-angiotensin system inhibitors.