Dietary Sodium Restriction: A Therapeutic Opportunity in CKD
Dietary Sodium Restriction: A Therapeutic Opportunity in CKD
Observational data from various studies, showing a J-curve between sodium intake and renal and cardiovascular outcome, have raised concern on the safety of rigorous sodium restriction. These observational data should be interpreted with caution, as a habitual salt intake below 5 g daily is a rarity in the outpatient population, and may well be an indicator of concomitant conditions compromising nutritional status as well as outcome. Moreover, quantification of sodium intake was questionable in some of the studies, by lack of 24-h urine data on sodium intake. This may have contributed to the substantial differences in the level of the nadir of the J-curve. Obviously, this debate is seriously hampered by a lack of prospective long-term sodium intervention data in CKD. Nevertheless, the presence of a J-curve has been reported in several independent studies (albeit not all) and should be given serious consideration. In experimental renal disease, we previously found that a regimen of ACEi and rigorous sodium restriction reduced blood pressure, proteinuria, and glomerular damage, but unexpectedly aggravated tubulo-interstitial damage. This was also found in healthy rats, so, it is not a particularity of the model but a generalizable adverse effect of the combination of RAAS-blockade or rigorous sodium restriction. This is disconcerting, as, moreover, the interstitial damage was not readily apparent from noninvasive parameters, so that if this occurred in patients it would go unnoticed. This once more underlines the need for better noninvasive markers of tubulo-interstitial damage. Considering the consistent association of interstitial damage with long-term renal outcome, this could provide a potential explanation for the association of very low sodium intake with worse renal outcome. Its mechanisms deserve further explanation, but could include intrarenal ischemia, excess reactive renin or aldosterone activation, or other causes.
Can We Go Too Low?
Observational data from various studies, showing a J-curve between sodium intake and renal and cardiovascular outcome, have raised concern on the safety of rigorous sodium restriction. These observational data should be interpreted with caution, as a habitual salt intake below 5 g daily is a rarity in the outpatient population, and may well be an indicator of concomitant conditions compromising nutritional status as well as outcome. Moreover, quantification of sodium intake was questionable in some of the studies, by lack of 24-h urine data on sodium intake. This may have contributed to the substantial differences in the level of the nadir of the J-curve. Obviously, this debate is seriously hampered by a lack of prospective long-term sodium intervention data in CKD. Nevertheless, the presence of a J-curve has been reported in several independent studies (albeit not all) and should be given serious consideration. In experimental renal disease, we previously found that a regimen of ACEi and rigorous sodium restriction reduced blood pressure, proteinuria, and glomerular damage, but unexpectedly aggravated tubulo-interstitial damage. This was also found in healthy rats, so, it is not a particularity of the model but a generalizable adverse effect of the combination of RAAS-blockade or rigorous sodium restriction. This is disconcerting, as, moreover, the interstitial damage was not readily apparent from noninvasive parameters, so that if this occurred in patients it would go unnoticed. This once more underlines the need for better noninvasive markers of tubulo-interstitial damage. Considering the consistent association of interstitial damage with long-term renal outcome, this could provide a potential explanation for the association of very low sodium intake with worse renal outcome. Its mechanisms deserve further explanation, but could include intrarenal ischemia, excess reactive renin or aldosterone activation, or other causes.
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