310
197 hemodialyzed patients with chronic kidney disease (with more than 6 months
vintage of hemodialysis therapy), it has been shown that among subjects with NE
plasma concentration located in third tertile, mean heart wall thickness was higher,
and concentric left ventricular hypertrophy was more prevalent then in patients from
two other tertiles. In these patients, plasma NE concentration was an independent
cardiovascular risk factor. In another study, it has been shown that patients undergo-
ing continuous ambulatory peritoneal dialysis (CAPD) have 3.5 times higher plasma
NE concentration than in healthy subjects. It is also important to stress that in
patients treated with CAPD, plasma NE concentration was 1.7 times higher than in
hemodialysis patients.
Results of animal experiments suggest that SNS overactivity participates in CKD
progression. Dorsal rhizotomy both in subtotally nephrectomized rats and in unine-
phrectomized Dahl salt-sensitive hypertensive rats prevents albuminuria and
glomerulosclerosis.
Given the pathophysiological evidence described above, the reduction of SNS
activity in CKD is a promising aim of therapy. In the recent years, two nonpharmaco-
logical interventional methods of such a treatment RDN and BAT were introduced.
Renal Denervation
The earliest invasive methods of hypertension treatment, introduced in 1920s, was
surgical thoracolumbar sympathectomy (splanchnicectomy). The operation proce-
dure leads to the section of sympathetic trunks along with removal great splanchnic
nerves from the celiac ganglion to mid-thoracic levels. This surgical early experi-
ence of 1226 splanchnicectomies was summarized by Smithwick et al. [ 8 ]. This
method reduced blood pressure and improved mortality but was characterized by
high surgical risk and led to severe long-term complications (urine and fecal incon-
tinence, erectile dysfunction, orthostatic hypotension) mainly due to extensive and
nonselective damage of SNS nerves, and therefore the use of this antihypertensive
treatment method was finally ceased. To avoid such complications, the methods of
more selective ablation of renal SNS nerves were needed. Before current status of
these methods will be described in this chapter, some data concerning anatomy of
renal nerves in humans should be given.
Kidney sympathetic innervation begins in intermediolateral column of the spinal
cord. Neuronal track leads from through pregangliotic fibers to sympathetic trunk
which includes splanchnic ganglia and then aortorenal ganglia. Sympathetic fibers
leave aortorenal ganglia as postgangliotic nerves run alongside with renal artery and
reach the kidney at the hilus. From this point, nerve fibers are dividing simultane-
ously with the divisions of arteries. It should be mentioned that in case of additional
renal arteries, the presence of parallel to these vessels sympathetic nerves was
revealed. Sakakura et al. investigated distribution of periarterial sympathetic nerve
fibers located around kidney arteries [ 9 ]. The autopsy studies showed that there
were fewer nerves surrounding the renal arteries in the distal segments compared
M. Adamczak et al.