title: Patiromer induces rapid and sustained potassium lowering in patients with chronic kidney disease and hyperkalemia.
abstract: Patients with chronic kidney disease (CKD) have a high risk of hyperkalemia, which increases mortality and can lead to renin-angiotensin-aldosterone system inhibitor (RAASi) dose reduction or discontinuation. Patiromer, a nonabsorbed potassium binder, has been shown to normalize serum potassium in patients with CKD and hyperkalemia on RAASi. Here, patiromer's onset of action was determined in patients with CKD and hyperkalemia taking at least one RAASi. After a 3-day potassium- and sodium-restricted diet in an inpatient research unit, those with sustained hyperkalemia (serum potassium 5.5 - under 6.5 mEq/l) received patiromer 8.4 g/dose with morning and evening meals for a total of four doses. Serum potassium was assessed at baseline (0 h), 4 h postdose, then every 2-4 h to 48 h, at 58 h, and during outpatient follow-up. Mean baseline serum potassium was 5.93 mEq/l and was significantly reduced by 7 h after the first dose and at all subsequent times through 48 h. Significantly, mean serum potassium under 5.5 mEq/l was achieved within 20 h. At 48 h (14 h after last dose), there was a significant mean reduction of 0.75 mEq/l. Serum potassium did not increase before the next dose or for 24 h after the last dose. Patiromer was well tolerated, without serious adverse events and no withdrawals. The most common gastrointestinal adverse event was mild constipation in two patients. No hypokalemia (serum potassium under 3.5 mEq/l) was observed. Thus, patiromer induced an early and sustained reduction in serum potassium and was well tolerated in patients with CKD and sustained hyperkalemia on RAASis.
authors.affiliation: Division of Nephrology, University of Rochester School of Medicine, Rochester, New York, USA.
authors.forename: David A
authors.initials: DA
authors.lastname: Bushinsky
authors.affiliation: Department of Medicine - Endocrinology, Brigham and Women's Hospital, Harvard Medical School, Harvard University, Boston, Massachusetts, USA.
authors.forename: Gordon H
authors.initials: GH
authors.lastname: Williams
authors.affiliation: University of Michigan School of Medicine, Ann Arbor, Michigan, USA.
authors.forename: Bertram
authors.initials: B
authors.lastname: Pitt
authors.affiliation: Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Weir
authors.affiliation: Department of Medicine, Massachusetts General Hospital, Harvard University, Boston, Massachusetts, USA.
authors.forename: Mason W
authors.initials: MW
authors.lastname: Freeman
authors.affiliation: Relypsa, Redwood City, California, USA.
authors.forename: Dahlia
authors.initials: D
authors.lastname: Garza
authors.affiliation: Relypsa, Redwood City, California, USA.
authors.forename: Yuri
authors.initials: Y
authors.lastname: Stasiv
authors.affiliation: PharmaStat, Newark, California, USA.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Li
authors.affiliation: Relypsa, Redwood City, California, USA.
authors.forename: Lance
authors.initials: L
authors.lastname: Berman
authors.affiliation: Comprehensive Hypertension Center, University of Chicago Medicine, Chicago, Illinois, USA.
authors.forename: George L
authors.initials: GL
authors.lastname: Bakris