Potassium Binding for Conservative and Preservative Management of Chronic Kidney Disease

Deborah J. Clegg; Biff F. Palmer


Curr Opin Nephrol Hypertens. 2020;29(1):29-38. 

In This Article

Abstract and Introduction


Purpose of review: Hyperkalemia is a life-threatening complication of chronic kidney disease (CKD). Risk factors include advanced kidney impairment, diabetes, hypertension, heart failure, and consumption of a K+-enriched diet. High-K+ diets provide health benefits to include reductions in blood pressure, stroke risk, and osteoporosis. Individuals at the highest risk for developing hyperkalemia are those who would benefit most from high K+ diets. Inhibitors of the renin--angiotensin--aldosterone system (RAASi) are effective in reducing cardiovascular events and slowing the progression of CKD, yet hyperkalemia is a risk factor. Discussed are new strategies facilitating use of both high-K+ diets and pharmacology to preserve kidney function and reduce cardiovascular events.

Recent findings: Sodium zirconium cyclosilicate and patiromer are new K+-binding drugs approved for the treatment of hyperkalemia. Both are efficacious in the short-term and long-term treatment of hyperkalemia. These binders are effective in treating hyperkalemia while facilitating RAASi therapy.

Summary: Hyperkalemia is a life-threatening condition. New K+-binding drugs allow for optimal use of pharmacological therapy, such as RAASi, enhancing their cardiorenal protection. Health benefits from consumption of high K+ foods may also be enhanced by use of these binders. In conclusion, there are new well tolerated and effective K+-binding agents for acutely and chronically managing hyperkalemia.


Hyperkalemia is a potentially serious medical condition, which can result in cardiac arrhythmia and sudden death. Risk factors include advanced stages of chronic kidney disease (CKD), heart failure, resistant hypertension, type 2 diabetes mellitus, myocardial infarction, and use of renin–angiotensin–aldosterone system inhibitors (RAASi).[1] RAASi therapy is associated with improved survival in patients with cardiovascular disease and decreased rates of decline in kidney function in both diabetic and nondiabetic CKD patients. However, the survival and other potential clinical benefits of RAASi therapy in patients must be weighed against their propensity to cause hyperkalemia placing clinicians in a catch 22 with respect to use of these drugs. If hyperkalemia develops following the initiation or use of RAASi therapy, clinicians are quick to reduce or discontinue their use resulting in many patients receiving suboptimal doses and/or discontinued therapy. There are new and novel treatment options available for individuals at risk for hyperkalemia. Here we briefly review normal K+ homeostasis, mechanisms by which hyperkalemia develops, and the utility of newly approved K+-binding drugs. We conclude by discussing how use of these binders may provide opportunities to maximize the dose of therapies that provide cardiorenal benefit while minimizing the risk of hyperkalemia.