Dietary sodium restriction: a neglected therapeutic opportunity in chronic kidney disease

Abstract

Purpose of review: Restriction of dietary sodium is recommended at a population level as well as for groups at high cardiovascular risk, and chronic kidney disease (CKD). This review addresses recent evidence for the protective effect of dietary sodium restriction in CKD patients specifically.

Recent findings: Sodium intake in CKD populations is generally high, and often above population average. Recent data demonstrated that moderately lower sodium intake in CKD patients is associated with substantially better long-term outcome of renin-angiotensin-aldosterone system (RAAS)-blockade, in diabetic and nondiabetic CKD, related to better effects of RAAS-blockade on proteinuria, independent of blood pressure. This is in line with better short-term efficacy of RAAS-blockade during moderate sodium restriction in diabetic and nondiabetic CKD. This effect of sodium restriction is likely mediated by its effects on volume status. Sustainable sodium restriction can be achieved by approaches on the basis of behavioral sciences.

Summary: Moderate restriction of dietary sodium can substantially improve the protective effects of RAAS-blockade in CKD, by specific renal effects apparent from proteinuria reduction. The latter precludes straightforward extrapolation of data from nonrenal populations to CKD. Concerns regarding the adverse effects of a very low sodium intake should not distract from the protective effects of moderate sodium restriction. Prospective studies should assess the efficacy and sustainability of different strategies to target high sodium intake in CKD, along with measures at population level.

Video abstract: http://links.lww.com/CONH/A14.

Box 1

no caption available

FIGURE 1

Sodium excretion (upper panel) during four different 6-week treatment periods by a rotation schedule in patients with diabetes and CKD on ACE-inhibitor therapy. NS intake was very high and accordingly also during SR without and with hydrochlorothiazide, sodium intake remained above recommended levels. Nevertheless, proteinuria (lower panel) was reduced significantly, as was blood pressure (data not shown). CKD, chronic kidney disease; HCT, hydrochlorothiazide; NS, normal sodium; SR, sodium restriction. Adapted from [^▪▪].

FIGURE 2

Renal survival in patients on ACEi by tertile of salt intake LSD 7.1 g/day, MSD 10.8 g/day, and HSD 14.2 g/day. ESRF, end stage renal failure; HSD, high sodium diet; LSD, low sodium diet; MSD, medium sodium diet. Adapted from [6].

FIGURE 3

Effect of sodium intake by tertile of urinary Na/creatinine (Cr) on the treatment benefit of ARB for renal (upper panels) and cardiovascular (lower panels) outcome in patients with type 2 diabetes and nephropathy. Urinary sodium excretion in the subsequent tertiles corresponded to a dietary salt intake of 8.9, 10.9, and 12.2 g, respectively. ARB, angiotensin-receptor blocker; RAAS, renin–angiotensin–aldosterone system. Adapted from [4].

FIGURE 4

Predictive value of NT-proBNP at baseline (untreated) for the responses of blood pressure (left panel) and proteinuria (right panel) to ARB, add-on sodium restriction, and add-on sodium restriction plus diuretic. NT-proBNP above the upper level of normal (>125 pg/ml) was not associated with the response to ARB, but predicted a more pronounced response to volume intervention by sodium restriction and thiazide. A similar predictive value of NT-proBNP for clinical efficacy of volume intervention was found for NT-proBNP during monotherapy ARB (not shown). ARB, angiotensin-receptor blocker; LS, low sodium. Adapted from [32].