Despite recent therapeutic advances, chronic kidney disease (CKD) is one of the fastest growing global causes of death. This illustrates limitations of current therapeutic approaches and, potentially, unidentified knowledge gaps. For decades, renin-angiotensin-aldosterone system blockers (RAAS) have been the mainstay of therapy for CKD. However, they favor the development of hyperkalemia that that is already common in CKD patients due to the CKDassociated decrease in urinary potassium (K + ) excretion and metabolic acidosis. Hyperkalemia may itself be life-threatening as it may trigger potentially lethal arrhythmia, and additionally may limit the prescription of RAAS blockers and lead to low K + diets associated to low dietary fiber intake. Indeed, hyperkalemia is associated with adverse kidney, cardiovascular and survival outcomes. Recently, novel kidney protective therapies, ranging from sodium/glucose cotransporter 2 (SGLT2) inhibitors to new mineralocorticoid receptor antagonists have shown efficacy in clinical trials. Herein, we review K + pathophysiology and the clinical impact and management of hyperkalemia considering these developments and the availability of the novel K + binders patiromer and sodium zirconium cyclosilicate, recent results from clinical trials targeting metabolic acidosis (sodium bicarbonate, veverimer) and an increasing understanding of the role of the gut microbiota in health and disease.
Key points-Hyperkalemia is a potentially lethal consequence of CKD.-Some commonly used treatments in CKD patients, like inhibitors of the RAAS system, have a potential effect worsening hyperkalemia -New treatments available in the nephrologist's armamentarium can be used in order to maintain K levels in the safe range Declarations: