Abstract. Obesity disproportionately elevates the risk of cardiorenal pathologies in the female sex, underscoring distinct, sex-specific mechanisms. Adipose tissue dysfunction, particularly in visceral depots, initiates a state of chronic, lowgrade inflammation, characterized by aberrant secretion of pro-inflammatory adipokines (e.g., leptin) and cytokines (e.g., IL-6, TNF-α). This inflammatory milieu, coupled with enhanced oxidative stress and renin-angiotensin-aldosterone system (RAAS) activation, is central to end-organ damage. Cardiac remodelling often culminates in a higher prevalence of heart failure with preserved ejection fraction, while the kidney undergoes maladaptive changes, including glomerular hyperfiltration and subsequent glomerulomegaly, accelerating progression toward chronic kidney disease. The post-menopausal loss of estrogen further amplifies this cardiorenal susceptibility by promoting a central fat distribution and metabolic derangement. This review integrates evidence on these differential pathways, stressing the imperative for tailored, precision-based strategies addressing adipose inflammation to mitigate the growing cardiorenal burden in women.
Key words. Obesity, estrogens, menopause, heart failure, chronic kidney disease.