261Blood Pressure Targets in CKD
In recent years, there are a number of guidelines in medical literature providing
recommendations for the management of high BP in HT including patients with
CKD [ 16 – 20 ]. The potential danger in such guidelines resides in the fact that they
focus on setting a BP threshold for treatment yet harm may exist with overtreatment
of HTN in patients with CKD. In a cohort of over 650,000 Veteran Americans with
CKD, extremes of both high and low BPs were associated with increased mortality,
with the highest mortality for patients with high pulse pressures. The authors con-
clude that it may not be advantageous to achieve an ideal systolic BP (<130 mm Hg)
in patients who have existing low diastolic BP (<70 mm Hg) [ 21 ].
Looking at this perspective, it is surprising to realize that there is still no suffi-
cient evidence to recommend a lower BP goal less than 140/90 mm Hg in patients
with CKD [ 8 ]. It is also a fact that, though some evidence informing the best treat-
ment BP target in CKD is available, not all groups looking at the same data agree on
exactly what the evidence shows.
The other important issue in CKD is the presence of albuminuria/proteinuria,
and increased urine protein/albumin excretion needs extra level of consideration
[ 22 ]. Thus the Kidney Disease Improving Global Outcomes BP work group advised
a lower BP goal of less than 130/80 mm Hg for individuals with CKD and moderate-
to- severe albuminuria (e.g., urine albumin-to-creatinine ratio > 30 mg/g) [ 23 ].
However, as suggested this recommendation was based on an evidence level equiva-
lent to expert opinion.
Thus studies especially interventional ones are still needed to determine which
BP values are optimal for better health outcomes in CKD patients.
Salt and Resistant Hypertension in CKD: Pathophysiologic View
The detailed pathophysiologic explanation for the RHT is beyond the scope of this
chapter. However, a brief explanation will be useful. Before beginning, it is impor-
tant to remember that the exact pathobiology of RHT is not known, although many
factors are thought to play a role. These include increased reduced renal mass, age,
arterial stiffness, vascular calcification and endothelial dysfunction, presence of dia-
betes, increased sympathetic nervous system activation renin angiotensin aldoste-
rone system (RAAS) imbalance, and altered sodium chloride handling in the distal
nephron or some combination of the earlier mentioned conditions [ 24 ] (Fig. 16.1).
It is also well recognized that high dietary salt intake not only exacerbates HT in
patients with CKD but also has the potential to directly worsen kidney function.
Rats receiving a high salt diet show sustained increases in kidney levels of
transforming growth factor-β, polypeptides associated with kidney fibrosis [ 25 ].
Since this chapter is primarily focused on RHT in CKD, from now on we will
explain this issue in more detail.
16 Treatment of Hypertension in Light of the New Guidelines: Salt Intake