Cardiorenal Syndrome: From Hemodynamic and Humoral Pathophysiology to New Frontiers in Modulation and Enabling Therapy—Part 2

Abstract

The therapeutic landscape of cardiorenal syndrome (CRS) has evolved significantly, transitioning from historical cornerstones like angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) to modern neurohormonal modulation with angiotensin receptor–neprilysin inhibitors (ARNIs). This second part of this narrative review analyzes the pivotal pharmacological roles of sodium–glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and finerenone, which target the hemodynamic, metabolic, and inflammatory–fibrotic axes, respectively, alongside the essential utility of novel potassium binders. Ultimately, the management of CRS is shifting toward an integrated cardiovascular–renal–metabolic paradigm, where the future lies in a personalized, biomarker-guided “quadruple cardiorenal therapy” that moves beyond a single-organ focus to optimize patient outcomes.