264
A recent systematic review also demonstrated that worsened kidney function,
defined as a decline in creatinine clearance, doubling of serum creatinine, or pro-
gression to end-stage renal disease, is associated with high sodium intake compared
to a low sodium intake [ 37 ].
Other proofs regarding salt and HT include reduced salt intake which is associ-
ated with an enhanced response to antihypertensive therapy [ 38 ] and high salt intake
that diminishes nighttime dipping of BP in salt-sensitive HT [ 39 ].
Thus all these data suggest that salt has an extraordinary role in development,
maintenance, and resistance of HT in CKD. Indeed, it was suggested that salt and
water balance in the kidney plays a role as the central long-term regulator of BP and
one can reasonably attribute a large portion of HTN in CKD to an impaired salt
excretion that is exacerbated by excess salt intake [ 24 ].
In sum, all of these findings suggest that there is very close relationship between
salt and RHT in CKD [ 29 , 40 ].
In the next section we will summarize the performed studies regarding salt, RHT,
and CKD.
Studies
Despite all these extensive research, it is very surprising to find that there are very
few studies regarding salt intake, salt restriction, and BP in CKD patients [ 41 ]. The
studies are mostly observational, have low patients numbers, and lack of control
groups. Therefore, as suggested above, the recommendation for sodium restriction
in the treatment of hypertension in CKD and in the reduction of cardiovascular and
overall mortality in CKD patients remains largely opinion-based.
Yu et al. investigated the role of dietary sodium intake on BP control among non-
dialysis Chinese CKD patients. They included 176 non-dialysis hypertensive CKD
patients. Sodium intake was measured by 24-h urine sodium excretion (24-h UNa).
Additionally, 20 patients with immunoglobulin A nephropathy (IgAN) participated
in a 7-day sodium restriction study (100 mmol/day). The average 24-h UNa of the
study cohort was 149.0 ± 66.4 mmol/day. The OR for each 17 mmol increment in
Table 16.1 The potential mechanisms related with increased salt and development of HT in CKD
↑ in extracellular volume and glomerular hypertension
↑ effect of vasoconstrictor substances and ↓ the effect of vasodilator substances
↑ sympathetic activity
Potentially ↑ the structural and functional pathologies in the vessel wall (vascular sclerosis,
endothelial dysfunction)
↑ oxidative stress
↑ urinary protein and albumin excretion
Blunts the effect of antihypertensive drugs (diuretics, ACE inhibitors, etc.)
↑ transforming growth factor-β production and kidney fibrosisB. Afsar and A. Kirkpantur