Abstract
<jats:title>Abstract</jats:title> <jats:p>Chronic kidney disease (CKD), defined per the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines by persistent (≥3 months) abnormalities of kidney structure or function, including reduced estimated glomerular filtration rate (eGFR) and/or albuminuria, affects 10%–15% of adults worldwide and is a powerful, independent risk factor for cardiovascular diseases, including heart failure (HF). In CKD (stages G1–G3), particularly when accompanied by albuminuria (KDIGO stages A2–A3), even mild reductions in eGFR are associated with subclinical cardiac abnormalities—left ventricular hypertrophy, concentric remodelling, LV diastolic dysfunction, HF with preserved ejection fraction, and arrhythmias. Many CKD patients meet criteria for Stage B HF within the contemporary ‘pre-HF’ framework, based on structural and functional cardiac alterations and elevated biomarkers in the absence of symptoms. Detection is here challenging, as symptoms are non-specific and circulating biomarkers are confounded by reduced renal clearance. Echocardiography, including speckle-tracking techniques and emerging indices, and cardiac magnetic resonance imaging with tissue characterization and strain analysis are sensitive tools for early diagnosis and risk stratification, but routine screening is not currently recommended in asymptomatic CKD. This condition may be mitigated by aggressive control of traditional and CKD-specific risk factors, and therapies with proven cardiorenal benefits—SGLT2 inhibitors, finerenone, diuretics, renin–angiotensin system blockers, and selected GLP-1 receptor agonists—guide HF prevention. Future research should test cost-effective early diagnostic strategies, clarify the role of imaging and biomarkers in guiding therapy, and exploit multiomics and artificial intelligence to unravel mechanistic heterogeneity and enable personalized prevention of HF in early CKD.</jats:p>