Addressing Renal Sodium Avidity in Chronic Heart Failure: There Is Always More than One Way to Skin a Cat.

BACKGROUND

Renal sodium avidity is a defining characteristic of chronic cardiorenal syndrome (CRS), leading to persistent sodium retention despite significant fluid overload. This phenomenon exacerbates volume overload, contributes to hemodynamic instability, and accelerates the decline of cardiac and renal function. Conventional diuretic therapies, though effective in acute settings, often fail chronically due to neurohormonal activation, renal tubular adaptations, and diuretic resistance.

SUMMARY: This review explores innovative approaches to overcoming natriuresis and diuresis resistance in CRS patients. Emerging pharmacological treatments, including sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor (GLP-1R) agonists, show potential in enhancing sodium excretion. Additionally, extracorporeal techniques such as ultrafiltration (UF) via hemodialysis and peritoneal dialysis (PD) provide precise sodium and fluid removal, bypassing many of the limitations of traditional pharmacotherapy. PD, in particular, has demonstrated efficacy in refractory cases by preserving residual renal function and improving diuretic responsiveness. As the saying goes, "there's always more than one way to skin a cat."

KEY MESSAGES: (1) Renal sodium avidity plays a crucial role in CRS progression, necessitating targeted interventions. (2) Standard diuretic therapies often fail to provide sustained relief due to compensatory mechanisms. (3) Novel pharmacological agents (SGLT2 inhibitors, GLP-1R agonists) and extracorporeal techniques (UF, PD) offer promising alternatives for managing sodium retention and fluid overload. (4) A multidisciplinary and personalized treatment strategy is essential for optimizing patient outcomes and improving quality of life.