In
Chronic Kidney Disease (CKD) patients, elevated blood pressure (BP) is a frequent finding and is traditionally considered a direct consequence of their
sodium sensitivity. Indeed,
sodium and fluid retention, causing hypervolemia, leads to the development of
hypertension in CKD. On the other hand, in non-dialysis CKD patients,
salt restriction reduces BP levels and enhances anti-proteinuric effect of renin-angiotensin-aldosterone system inhibitors in non-dialysis CKD patients. However, studies on the long-term effect of
low salt diet (
LSD) on cardio-renal prognosis showed controversial findings. The negative results might be the consequence of measurement bias (spot urine and/or single measurement), reverse epidemiology, as well as poor adherence to diet. In
end-stage kidney disease (ESKD), dialysis remains the only effective means to remove
dietary sodium intake. The mismatch between intake and removal of
sodium leads to fluid overload,
hypertension and
left ventricular hypertrophy, therefore worsening the prognosis of ESKD patients. This imposes the implementation of a
LSD in these patients, irrespective of the lack of trials proving the efficacy of this measure in these patients.
LSD is, therefore, a rational and basic tool to correct fluid overload and
hypertension in all CKD stages. The implementation of
LSD should be personalized, similarly to
diuretic treatment, keeping into account the volume status and true burden of
hypertension evaluated by ambulatory BP monitoring.