Purpose of review: To evaluate the role of restricting dietary sodium intake in chronic kidney disease (CKD) and its complications.
Recent findings: A consistent line of evidence shows that high dietary sodium intake is a determinant of therapy resistance to blockade of the renin-angiotensin-aldosterone system (RAAS). Addition of sodium restriction to RAAS blockade or to RAAS blockade combined with a diuretic permits a further reduction in urinary protein excretion of approximately 30%, which could be expected to reduce long-term renal risk by 25%.
Summary: High sodium intake increases blood pressure and proteinuria, induces glomerular hyperfiltration and blunts the response to RAAS blockade. Although recommended in international guidelines, sodium restriction is not a spearhead in treating renal patients. Sodium status is only rarely mentioned in recent large intervention studies in CKD. Sodium intake in CKD is similar to that in the general population. Reduction of sodium intake to the target of 50-85 mmol/24 h in patients with CKD reduces blood pressure and proteinuria, the latter by approximately 30%, and should be actively pursued to improve outcome in CKD.