TY - JOUR
T1 - Potassium Binders for Hyperkalemia in Chronic Kidney Disease—Diet, Renin-Angiotensin-Aldosterone System Inhibitor Therapy, and Hemodialysis
AU - Palmer, Biff F.
N1 - Publisher Copyright:
© 2019 Mayo Foundation for Medical Education and Research
PY - 2020/2
Y1 - 2020/2
N2 - Hyperkalemia is a potentially life-threatening complication of chronic kidney disease (CKD). The management of CKD requires balancing the benefits of specific treatments, which may exacerbate the potential for hyperkalemia, with the risks of hyperkalemia itself. Renin-angiotensin-aldosterone system (RAAS) inhibitors, which slow CKD progression and improve cardiovascular outcomes, are often discontinued if hyperkalemia develops. Patients with hyperkalemia are frequently advised to restrict dietary potassium (K+), depriving these patients of many heart-healthy foods. Patients receiving hemodialysis are particularly susceptible to hyperkalemia during long interdialytic intervals, and managing this risk without causing hypokalemia can be challenging. Recently, 2 K+-binding agents were approved for the treatment of hyperkalemia: sodium zirconium cyclosilicate and patiromer. These agents offer alternatives to sodium polystyrene sulfonate, which is associated with serious gastrointestinal adverse effects. For this review, PubMed was searched for English-language articles published in 2014-2018 using the terms patiromer, sodium zirconium cyclosilicate, sodium polystyrene sulfonate, hyperkalemia, renin-angiotensin-aldosterone, diet, and dialysis. In randomized controlled studies of patients with hyperkalemia, sodium zirconium cyclosilicate and patiromer effectively reduced serum K+ and were generally well tolerated. Furthermore, patients in these studies could maintain RAAS inhibitor therapy and, in some studies, were not required to limit dietary K+. There may also be a role for these agents in preventing hyperkalemia in patients receiving hemodialysis. Thus, K+-binding agents may allow patients with CKD at risk for hyperkalemia to optimize RAAS inhibitor therapy, receive benefits of a K+-rich diet, and experience improved hemodialysis outcomes. Additional long-term studies are necessary to confirm these effects.
AB - Hyperkalemia is a potentially life-threatening complication of chronic kidney disease (CKD). The management of CKD requires balancing the benefits of specific treatments, which may exacerbate the potential for hyperkalemia, with the risks of hyperkalemia itself. Renin-angiotensin-aldosterone system (RAAS) inhibitors, which slow CKD progression and improve cardiovascular outcomes, are often discontinued if hyperkalemia develops. Patients with hyperkalemia are frequently advised to restrict dietary potassium (K+), depriving these patients of many heart-healthy foods. Patients receiving hemodialysis are particularly susceptible to hyperkalemia during long interdialytic intervals, and managing this risk without causing hypokalemia can be challenging. Recently, 2 K+-binding agents were approved for the treatment of hyperkalemia: sodium zirconium cyclosilicate and patiromer. These agents offer alternatives to sodium polystyrene sulfonate, which is associated with serious gastrointestinal adverse effects. For this review, PubMed was searched for English-language articles published in 2014-2018 using the terms patiromer, sodium zirconium cyclosilicate, sodium polystyrene sulfonate, hyperkalemia, renin-angiotensin-aldosterone, diet, and dialysis. In randomized controlled studies of patients with hyperkalemia, sodium zirconium cyclosilicate and patiromer effectively reduced serum K+ and were generally well tolerated. Furthermore, patients in these studies could maintain RAAS inhibitor therapy and, in some studies, were not required to limit dietary K+. There may also be a role for these agents in preventing hyperkalemia in patients receiving hemodialysis. Thus, K+-binding agents may allow patients with CKD at risk for hyperkalemia to optimize RAAS inhibitor therapy, receive benefits of a K+-rich diet, and experience improved hemodialysis outcomes. Additional long-term studies are necessary to confirm these effects.
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U2 - 10.1016/j.mayocp.2019.05.019
DO - 10.1016/j.mayocp.2019.05.019
M3 - Review article
C2 - 31668450
AN - SCOPUS:85074511307
SN - 0025-6196
VL - 95
SP - 339
EP - 354
JO - Mayo Clinic Proceedings
JF - Mayo Clinic Proceedings
IS - 2
ER -