Body Fluid-Independent Effects of Dietary Salt Consumption in Chronic Kidney Disease

Abstract

The average dietary salt (i.e., sodium chloride) intake in Western society is about 10 g per day. This greatly exceeds the lifestyle recommendations by the WHO to limit dietary salt intake to 5 g. There is robust evidence that excess salt intake is associated with deleterious effects including hypertension, kidney damage and adverse cardiovascular health. In patients with chronic kidney disease, moderate reduction of dietary salt intake has important renoprotective effects and positively influences the efficacy of common pharmacological treatment regimens. During the past several years, it has become clear that besides influencing body fluid volume high salt also induces tissue remodelling and activates immune cell homeostasis. The exact pathophysiological pathway in which these salt-induced fluid-independent effects contribute to CKD is not fully elucidated, nonetheless it is clear that inflammation and the development of fibrosis play a major role in the pathogenic mechanisms of renal diseases. This review focuses on body fluid-independent effects of salt contributing to CKD pathogenesis and cardiovascular health. Additionally, the question whether better understanding of these pathophysiological pathways, related to high salt consumption, might identify new potential treatment options will be discussed.

Keywords: chronic kidney disease; fibrosis; inflammation; microcirculation; salt; tissue sodium storage.

Figure 1

The direct harmful effects of salt on kidney tissue remodeling, kidney microvasculature and renal inflammation.

Figure 2

Different mechanisms of sodium handling and their effects on the human body with regard to possible treatment targets (either life-style or pharmacologically mediated). Below the dotted line the mechanisms associated with non-osmotic sodium storage are visualized, for these mechanisms further research into potential treatment targets is necessary.