Blog entry by Arif Khwaja
So after analysing the effect of obesity and phosphorus yet another post-hoc analysis from the REIN study is about to be published in JASN ! This analysis looked at the effect of dietary salt intake (as measured by 24 hour urinary sodium and creatinine) suggests that those with high salt intake were more likely to progress to ESRD and that this was mediated by attenuating the anti-proteinuric effects of ACE-I. Among those with low, medium, and high sodium intakes, the incidence of ESRD was 6.1 %, 7.9 and 18.2 per 100 patient-years, respectively (P<0.001). Somewhat counter-intuitively there was no difference in blood pressure and the association between salt intake and progression was lost when taking into account changes in proteinuria during follow up - leading the authors to conclude that the anti-proteinuric effects of ACE-i were mitigated by salt intake.The authors suggest that expansion of the sodium pool leads to glomerular hyperfiltration and activation of the renal RAS ithereby mitigating the anti-proteinuric effects of ACEi.
It has been established for many years that diuretics and salt restriction both augment the anti-hypertensive effects of ACE-i and so it is surprising to see no difference in BP between the hogh and low sodium groups. As said before I am never comfortable with the use of post-hoc analysis to try to elucudate the mechanism of action of a drug or a treatment recommendation. However the article reinforces the need salt restriction in the CKD population and the importance of factoring salt intake into any trials of progression. Whilst salt restriction is clearly important I'm not sure I share the authors belief that salt restriction can be achieved easily by 'small inconveniences of minimal dietary restrictions" - my personal experiene is that all dietary interventions are difficult to achieve and require considerable dietic resource.