[Role of inflammation in heart failure with preserved ejection fraction: from nephro-metabolic interactions to future therapeutic implications].

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical entity frequently associated with chronic kidney disease (CKD). Recent studies indicate that 50-60% of HFpEF patients also have CKD, and the prevalence of HFpEF among CKD patients is similarly high. Chronic low-grade systemic inflammation is common to both conditions and is linked to risk factors such as obesity, insulin resistance, and diabetes. The hyperactivation of the mineralocorticoid receptor plays a central role in this process, contributing to interstitial fibrosis and inflammation. Additional factors, including metabolic acidosis, gut dysbiosis, and reduced expression of the α-Klotho protein, amplify the inflammatory response. This systemic inflammation reduces nitric oxide production, impairing cardiac diastolic function and, together with metabolic syndrome and aging, further exacerbates the already complex cardiac pathology. Therapeutic strategies aimed at reducing inflammation, such as renin-angiotensin-aldosterone system inhibitors and sodium-glucose cotransporter 2 inhibitors, show promising potential. Additionally, the use of anti-inflammatory drugs and novel interventions to restore gut microbiota balance may offer new opportunities to improve prognosis in patients with HFpEF and CKD. Further studies are needed to clarify the clinical efficacy of these approaches and their role in optimizing the management of this complex patient population.