Secondary Prevention of Hyperkalemia With Sodium Polystyrene Sulfonate in Cardiac and Kidney Patients on Renin-Angiotensin-Aldosterone System Inhibition Therapy
Article first published online: 6 NOV 2011
© 2011 Wiley Periodicals, Inc.
Volume 35, Issue 1, pages 32–36, January 2012
How to Cite
Chernin, G., Gal-Oz, A., Ben-Assa, E., Schwartz, I. F., Weinstein, T., Schwartz, D. and Silverberg, D. S. (2012), Secondary Prevention of Hyperkalemia With Sodium Polystyrene Sulfonate in Cardiac and Kidney Patients on Renin-Angiotensin-Aldosterone System Inhibition Therapy. Clin Cardiol, 35: 32–36. doi: 10.1002/clc.20987
- Issue published online: 10 JAN 2012
- Article first published online: 6 NOV 2011
- Manuscript Accepted: 5 SEP 2011
- Manuscript Received: 28 JUN 2011
Hyperkalemia, induced by renin-angiotensin-aldosterone system inhibition (RAAS-I) in patients with chronic kidney disease (CKD), or cardiac disease often leads to withdrawal of RAAS-I therapy. Sodium polystyrene sulfonate (SPS) is a potassium-binding resin used for the treatment of hyperkalemia. Recently, concerns about the safety and efficacy of SPS were raised. We report here a follow-up of 14 patients with CKD and heart disease on RAAS-I treatment who were treated with low-dose daily SPS to prevent recurrence of hyperkalemia.
Daily SPS is safe and effective for secondary prevention of hyperkalemia induced by RAAS-I therapy in CKD patients with heart disease.
We reviewed the medical charts of the patients with CKD (nondialysis patients) and heart disease treated in our CKD clinic from 2005 to 2010 and identified all patients on RAAS-I therapy who were treated with daily SPS (sorbitol-free) after episodes of hyperkalemia. Data on hospitalizations, symptoms that may be attributed to SPS therapy, and electrolyte concentration levels were obtained.
Fourteen patients were treated with low-dose SPS therapy for a total of 289 months (median length of follow-up, 14.5 months). None of the patients developed colonic necrosis or life-threatening events that could be attributed to SPS use. Mild hypokalemia was noted in 2 patients and responded to reducing the dose of SPS. No further episodes of hyperkalemia were recorded while patients were on the therapy. SPS was well-tolerated during the follow-up without need for withdrawal or reduction of the dose of RAAS-I therapy by any patients.
Low-dose SPS was safe and effective as a secondary preventive measure for hyperkalemia induced by RAAS-I in CKD patients with heart disease. © 2011 Wiley Periodicals, Inc.
The authors have no funding, financial relationships, or conflicts of interest to disclose.