Resistant Hypertension in Chronic Kidney Disease

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MSNA in CKD patients undergoing hemodialysis after bilateral nephrectomy did
not differ from healthy subjects [ 1 ]. Hausberg et al. have proven that despite correc-
tion of uremia in patients after renal transplantation with adequate transplanted kid-
ney function but preserved native kidneys, MSNA is increased as in CKD
hemodialysis patients. MSNA in kidney transplant patients after bilateral nephrec-
tomy was comparable to healthy volunteers [ 2 ]. Increased MSNA has been also
reported in patients with autosomal dominant polycystic kidney disease (ADPKD)
even in the presence of a normal glomerular filtration rate (GFR). In another study,
Grassi et al. demonstrated that increased activation of SNS is present in the early
stages of CKD (mean estimated glomerular filtration rate – eGFR – in the studied
patients: 41 ml/min per 1.73 m^2 ) [ 3 ]. Results of the above-quoted clinical studies
suggest that SNS overactivity in CKD is caused by diseased kidneys themselves.
Results of the animal experiments confirmed such a hypothesis. Ye et al. showed
that applying a small lesion in one kidney by an intrarenal phenol injection, not
affecting kidney function, increases SNS activity and leads to a long-term increase
of noradrenaline secretion and arterial hypertension. These effects are abolished by
afferent surgical denervation [ 4 ]. It has been showed in subtotally nephrectomized
rats that blood pressure increase and elevation of norepinephrine (NE) turnover in
sympathetic brain centers was reduced by afferent surgical denervation (dorsal rhi-
zotomy, a procedure in which the dorsal roots from Th10-L2 were damaged).
The number of abovementioned evidence suggests that the kidneys are both
recipients and generators of increased SNS activity (Fig. 19.1). To explain this, a
short description of the function of the renal nerves should be given.
Kidneys are innervated by two types of fibers: (1) sensory afferent fibers leading
from the central nervous system (axons of the neurons located in thoracic and lum-
bar sympathetic trunks) to the kidneys and (2) sympathetic efferent fibers which
start in the kidneys and conduct nerve impulses to the central nervous system (cell
bodies localized ipsilateral Th6-L4 trunks). Both types of fibers localized along the
renal arteries in adventitia enter the kidneys at the hilum and extend to the vascular
and tubular compartments.

Efferent sympathetic

nerves

BLOOD PRESSURE

Efferent sympathetic

nerves

Afferent sympathetic

nerves

β 1 receptor - renin secretion β 1 receptor - cardiac output

α 1 receptor - Na+^ reabsorption α^1 - vasoconstriction heart rate

Fig. 19.1 The role of renal sympathetic nerves in blood pressure regulation

M. Adamczak et al.