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Possible Advantages Deriving from Patiromer Use in Hypertensive Patients Made Hyperkalemic by Renin–Angiotensin–Aldosterone Blocking Agents

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Abstract

Hyperkalemia is an elevated level of serum potassium (K+) and does represent a life-threatening condition. In clinical practice, hyperkalemia mainly derives from an impaired renal K+ excretion which, in turn, is usually caused by either acute or chronic renal failure. In concordance with this, hyperkalemia is very common in several chronic conditions, such as kidney disease, diabetes mellitus, heart failure, hypertension, and coronary heart disease. In all of these conditions the use of Renin–Angiotensin–Aldosterone System inhibitors (RAASIs), such as angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), and mineralocorticoid receptor antagonist is widely recommended and further increases the risk of hyperkalemia. As hypertension is concerned, clinical trials suggest that the risk of hyperkalemia associated with RAASIs ranges from 2 to 10%. This often leads to a reduction or complete cessation of RAASIs, leaving patients without protective medications. Patiromer, a new oral potassium-binding agent, has been approved for clinical use in several countries, including Europe and US. Clinical studies have demonstrated that patiromer is effective in inducing a rapid and sustained K+ reduction in various patient settings, including those where RAASIs are a fundamental component of cardiorenal protection. Patiromer is generally well tolerated and characterised by a good safety profile. Most importantly, patiromer use might allow the continuation of ACEIs and ARBs in hypertensive patients developing hyperkalemia during treatment and thereby favour a more effective and long-lasting cardiorenal protection.

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Correspondence to Claudio Ferri.

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Borghi, C., Ferri, C., Pontremoli, R. et al. Possible Advantages Deriving from Patiromer Use in Hypertensive Patients Made Hyperkalemic by Renin–Angiotensin–Aldosterone Blocking Agents. High Blood Press Cardiovasc Prev 28, 555–559 (2021). https://doi.org/10.1007/s40292-021-00478-2

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