Salt and chronic kidney disease

Disruption of sodium homeostasis has a central role in the development and progression of chronic kidney disease (CKD). Excess dietary sodium can overwhelm regulatory mechanisms and amplify pathways that promote kidney injury, hypertension and cardiovascular disease. In CKD, altered sodium handling has haemodynamic effects, leads to activation of the renin-angiotensin-aldosterone system and contributes to tissue sodium accumulation, endothelial dysfunction and inflammatory responses that further accelerate disease progression. Emerging evidence suggests that variability in these pathways - shaped by genetic predisposition and heterogeneous CKD phenotypes - may influence individual susceptibility to sodium-mediated damage and responses to therapeutic interventions. Although dietary sodium restriction remains a cornerstone of CKD management, improved understanding of sodium homeostasis as a multidimensional driver of CKD provides a broader framework for understanding disease mechanisms and may help to refine risk stratification and treatment strategies to enable maximal clinical benefit for patients at a high risk of sodium-mediated complications.