Dietary Salt Intake and Hypertension in Chronic Kidney Disease.

Abstract

There is a high prevalence of hypertension, which is both a cause and consequence of kidney function decline, among patients with chronic kidney disease (CKD). Impaired sodium excretion and the activation of the renin-angiotensin-aldosterone system (RAAS) are central mechanisms underlying this relationship. In early CKD, compensatory increases in fractional sodium excretion help maintain the balance of sodium in the body; however, as kidney function deteriorates, this compensatory mechanism is overwhelmed, resulting in sodium retention, extracellular volume expansion, and predominantly volume-dependent hypertension. Furthermore, CKD is characterized by heightened salt sensitivity, owing to which blood pressure (BP) responds disproportionately to changes in dietary salt intake. Emerging evidence suggests that non-osmotic sodium storage in tissues, such as alterations in glycosaminoglycan networks, impaired lymphatic clearance, and endothelial glycocalyx dysfunction, further contributes to salt-sensitive hypertension. Together with RAAS activation, these mechanisms promote vascular dysfunction, BP variability, and adverse cardiovascular outcomes. Dietary salt intake is a key modifiable factor in the management of CKD and hypertension. Randomized controlled trials have shown that decreased salt intake lowers BP, reduces proteinuria, and enhances the efficacy of RAAS inhibitors, thereby slowing the progression of CKD and reducing cardiovascular risk. Conversely, increased salt intake is associated with resistant hypertension, increased BP variability, and higher mortality; therefore, current guidelines recommend limiting salt intake to 5 g/day. The role of dietary potassium is increasingly recognized; however, caution is required in patients with advanced CKD due to the risk of hyperkalemia.