High sodium intake, whether via diet or drugs, augments cardiorenal risk. Regardless of its source, high sodium intake can both lead to hypertension and reduce the efficacy of renin-angiotensin-aldosterone system inhibitors, which are currently guideline-recommended treatments for hypertension, chronic kidney disease, and heart failure. Reducing sodium intake is therefore recommended to reduce the risk of adverse cardiorenal outcomes. An inverse relationship exists between sodium and potassium, with foods high in sodium being lower in potassium. Diets high in potassium have been associated with reducing hypertension and heart failure; however, optimal renin-angiotensin-aldosterone system inhibitor dosing is often limited by hyperkalemia, which can lead to life-threatening cardiac arrhythmias and increased mortality. Potassium binders are effective at reducing potassium levels. Although some use sodium as the potassium exchange ion, thus increasing sodium intake, a new potassium binder uses another exchange ion and therefore does not increase sodium intake. When treatment options require agents that may precipitate hyperkalemia, particularly in patients at high cardiorenal risk, drugs that do not add to the sodium load may be preferred. A literature search was conducted using PubMed; search terms included potassium, sodium, hyperkalemia, potassium binders, and the literature search focused on manuscripts published more recently since 2000.