Albuminuria in Heart Failure: From Marker to Modifiable Target

Albuminuria, once viewed solely as a renal biomarker, has emerged as an integrative indicator of endothelial dysfunction, vascular injury, and systemic congestion in heart failure (HF). Evidence now suggests it not only reflects disease severity but also contributes to the cardiorenal mechanisms that drive progression. Hemodynamic stress, glomerular glycocalyx disruption, and renin-angiotensin-aldosterone system activation promote albumin leakage through oxidative and inflammatory injury. Large studies such as BIOlogy Study to TAilored Treatment in Chronic Heart Failure and FINerenone trial to investigate Efficacy and sAfety supeRioR to placebo in paTientS with Heart Failure show that 40–50% of patients with HF exhibit albuminuria, which correlates with markers of congestion and independently predicts hospitalization and mortality in both reduced and preserved ejection fraction phenotypes. Even low-grade albuminuria is associated with increased cardiovascular risk, and changes in urinary albumin-to-creatinine ratio (uACR) over time track with outcomes. Therapies including mineralocorticoid receptor antagonists, sodium-glucose cotransporter 2 inhibitors, and renin-angiotensin-aldosterone system blockade can reduce albuminuria, though whether lowering uACR itself improves outcomes remains uncertain. Albuminuria bridges renal, vascular, and hemodynamic risk and may serve as both a biomarker and modifiable target in HF. Incorporating routine uACR measurement into clinical care could refine risk stratification and therapeutic monitoring, while future studies should clarify whether targeted albuminuria reduction yields meaningful improvements in HF outcomes.