What question did this study set out to answer?

The research aims to explore how aldosterone excess contributes to cardiovascular-kidney-metabolic syndrome and its management.

April 22, 2026

Hyperaldosteronism in the Pathophysiology and Management of Cardiovascular‐Kidney‐Metabolic Syndrome

Q: What is the clinical evidence from this study?

Study design: Review. Population: Cardiovascular-kidney-metabolic (CKM) syndrome. Intervention: Aldosterone-targeted therapies (RAAS inhibitors, MRAs, GLP-1 RAs).

Key Result

Inhibition of aldosterone signaling, including through mineralocorticoid receptor antagonists and GLP-1 receptor agonists, is a foundational treatment approach for managing CKM syndrome.

Key Points

The research aims to explore how aldosterone excess contributes to cardiovascular-kidney-metabolic syndrome and its management.
Analyzed the interplay of obesity, diabetes, chronic kidney disease, and cardiovascular disease in CKM syndrome.
Reviewed pharmacologic options addressing aldosterone signalling, including RAAS inhibitors and mineralocorticoid receptor antagonists.
Discussed potential of combination therapies for managing aldosterone excess.
Elevated aldosterone is linked to structural changes in kidneys and heart, worsening CKM syndrome.
Pharmacologic interventions effectively reduce aldosterone and improve outcomes in CKM patients.
The study emphasizes the need for further research into targeted therapies and patient subgroups.

Structured PICO

Population

Patients with Cardiovascular-kidney-metabolic (CKM) syndrome

Intervention

Aldosterone-targeted therapies (RAAS inhibitors, ARNIs, MRAs, aldosterone synthase inhibitors, GLP-1 RAs)

Obesity-induced aldosterone excess is a key pathophysiologic factor in CKM syndrome, making aldosterone-targeted therapies a pillar of management.

Abstract

ABSTRACT Cardiovascular‐kidney‐metabolic (CKM) syndrome is defined by the pathologic interconnections between obesity, diabetes, chronic kidney disease and cardiovascular disease. An important and underrecognized pathophysiologic factor underlying CKM syndrome is obesity‐induced 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‐angiotensin‐aldosterone system (RAAS) inhibitors, angiotensin receptor‐neprilysin inhibitors and steroidal (such as spironolactone) or non‐steroidal (currently only finerenone) mineralocorticoid receptor antagonists. Additionally, aldosterone synthase inhibitors are currently in development. Effective anti‐obesity medications such as glucagon‐like peptide‐1 receptor agonists inhibit aldosterone production due to their effects on adipocytes and in the kidneys. RAAS inhibition is also used to optimize the long‐term management of CKM syndrome. Future research should seek to characterize the benefits of combination therapies for aldosterone excess and determine which subgroups of patients most benefit from aldosterone‐targeted therapies.

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