Heart failure (HF) and chronic kidney disease (CKD) frequently coexist and amplify each other through tightly connected hemodynamic, neurohormonal, metabolic, and inflammatory pathways. This bidirectional interaction—conceptualized as Cardiorenal Syndrome (CRS)—represents one of the most challenging intersections in cardiovascular and renal medicine, contributing to high morbidity, therapeutic complexity, and poor survival. Venous congestion, rather than impaired cardiac output alone, is now recognized as the primary hemodynamic driver of renal dysfunction in HF. Neurohormonal activation, inflammation and endothelial injury further promote progressive cardiac and renal damage. Early detection using biomarkers, imaging modalities, and careful assessment of volume status is crucial for differentiating true kidney injury from functional or hemodynamic changes. Management requires a finely balanced approach aimed at relieving congestion, maintaining renal perfusion, and implementing guideline-directed medical therapy (GDMT), including RAAS inhibitors, β-blockers, mineralocorticoid receptor antagonists, and SGLT2 inhibitors. Modern strategies such as sequential nephron blockade, acetazolamide use, ultrafiltration, and peritoneal dialysis offer additional options for refractory congestion. Emerging concepts such as cardiovascular–kidney–metabolic (CKM) syndrome underscore the role of metabolic dysfunction in cardiorenal pathology. An integrated heart–kidney approach, incorporating personalized therapy and multidisciplinary care, is essential to improve long-term outcomes in this complex patient population.