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An important and underrecognized pathophysiologic factor underlying CKM syndrome is obesity\u2010induced aldosterone excess. This excess aldosterone causes structural and functional alterations in the kidneys, heart and vasculature promoting development of chronic kidney disease, cardiovascular disease and heart failure. Inhibition of aldosterone signalling is a pillar in the treatment approach to CKM syndrome. Pharmacologic options include renin\u2010angiotensin\u2010aldosterone system (RAAS) inhibitors, angiotensin receptor\u2010neprilysin inhibitors and steroidal (such as spironolactone) or non\u2010steroidal (currently only finerenone) mineralocorticoid receptor antagonists. Additionally, aldosterone synthase inhibitors are currently in development. Effective anti\u2010obesity medications such as glucagon\u2010like peptide\u20101 receptor agonists inhibit aldosterone production due to their effects on adipocytes and in the kidneys. RAAS inhibition is also used to optimize the long\u2010term management of CKM syndrome. 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