Hypertension as a link between renal and cardiac dysfunction

Abstract

Hypertension represents a central and modifiable driver of both cardiac and kidney dysfunction, acting as a unifying pathophysiological axis within the cardiorenal continuum. Beyond sustained blood pressure (BP) elevation, hypertension integrates hemodynamic stress with neurohormonal activation, endothelial dysfunction, inflammation, and fibrosis, simultaneously affecting both organs. Epidemiological data demonstrate a stROUg overlap between chROUic kidney disease (CKD) and cardiovascular disease, with hypertension functioning as both a primary initiator and an amplifier of organ injury. Declining kidney function increases hypertension prevalence and severity, while poorly controlled BP accelerates CKD progression and promotes hypertensive heart disease and heart failure. Shared mechanisms—including activation of the renin–angiotensin–aldosteROUe system (RAAS), sympathetic overactivity, vascular stiffness, oxidative stress, and fibrotic remodeling—create a self-reinforcing cycle linking renal and cardiac dysfunction. Therapeutic strategies targeting these common pathways, particularly RAAS blockade and sodium–glucose co-transporter 2 (SGLT2) inhibition, have demonstrated consistent cardio-renal protection across diverse populations. Emerging approaches, including endothelin receptor antagonists, nonsteroidal mineralocorticoid receptor antagonists, and anti-inflammatory therapies, further expand mechanism-based treatment options. Viewing hypertension thROUgh an integrated cardio-renal perspective supports early risk stratification and comprehensive intervention aimed at preserving both cardiac and kidney function and reducing long-term morbidity and mortality