315assessed by serum creatinine and cystatin C concentrations or eGFR was preserved
during 1 year follow-up. Nevertheless in some patients, slight decrease of eGFR
after RDN was observed. This worsening of renal function might be caused by pro-
cedure itself or was related to progression of hypertensive kidney disease. In
Symplicity HTN-2 study, the decrease of urine albumin-to-creatinine ratio (UACR)
6 months after RDN was shown [ 11 ]. Similarly, in the other clinical studies, a sig-
nificant decrease of albuminuria measured by UACR in resistant hypertension
patients treated with RDN was found.
There are three preliminary clinical studies evaluating the effect of RDN on kid-
ney function in CKD patients (Table 19.2). Hering et al. studied 15 patients with
stage 3–4 CKD (eGFR 31 ml/min.) and resistant hypertension. Taking into account
impaired kidney function in these studied patients, CO 2 angiography was performed.
It was revealed that renal function after RDN in this group of patients was preserved
during 1 year follow-up. In this study, RDN did not affect significantly proteinuria
[ 16 ]. Ott et al. in other clinical study in a group of 27 patients with stage 3–4 CKD
(eGFR 48 ml/min.) and resistant hypertension found that RDN slows decline of
renal function. They found significant annual difference in eGFR changes before
and 1 year after RDN (−5 vs +1.5 ml/min per 1.73 m^2 per year, respectively) [ 17 ].
Kiuchi et.al. had shown that patients with CKD stage 2-4, treated by renal denerva-
tion benefit not only by lowering the blood pressure but also improving kidney
function. RDN in 24-month observation led to renal function (measured by mean
eGFR) improvement by 42% and albuminuria decrease by 87% [ 18 ]. These promis-
ing results suggesting nephroprotective properties of RDN need to be however con-
firmed in larger studies.
Dörr et al. in resistant hypertension patients with preserved and slightly impaired
kidney function (i.e., with eGFR <45 ml/min/1.73 m^2 ) analyzed the influence of
RDN on acute kidney injury biomarkers (urinary concentrations of neutrophil
gelatinase- associated lipocain, NGAL, and kidney injury molecule – KIM-1). In
this study, no significant changes of eGFR and urinary NGAL and KIM-1 concen-
trations after RDN were found [ 19 ].
As SNS hyperactivity is one of the causes of blood pressure increase in CKD
patients, it raises the question whether RDN might be an effective antihypertensive
treatment in this group of patients. Hering et al. in already-quoted study had shown
that RDN is an effective antihypertensive treatment in patients with CKD stage 3–4
and resistant hypertension (mean blood pressure reduction 1 year after RDN was
33/19 mmHg) (Table 19.2). Additionally in this study, it was found that RDN sig-
nificantly decreased nighttime ABPM [ 16 ]. Similarly Ott et al. in other clinical
study in patients with CKD stage 3–4 and resistant hypertension found that RDN
leads to significant blood pressure reduction (1 year after RDN SBP reduction was
20 mmHg and DBP reduction was 8 mmHg) [ 17 ]. Case reports and results of small
observational study (12 patients) showed that RDN leads to blood pressure reduc-
tion also in hemodialysis CKD patients.
Besides antihypertensive properties, SNS afferent nerve disruption by RDN may
be advantageous in the case of renal pain control. In some patients with ADPKD,
chronic and abdominal, flank, or back pain is present due to enlarged cystic kidneys
19 Devices for Neural Modulation (Renal Denervation, Barostimulation)