Renal sympathetic nerve activity after catheter-based renal denervation

Catheter-based renal sympathetic denervation (RDN) has been considered a potential treatment for therapy resistant hypertension (RHT). However, in a randomized placebo-controlled trial, RDN did not lead to a substantial blood pressure (BP) reduction. We hypothesized that variation in the reported RDN efficacy might be explained by incomplete nerve disruption as assessed by renal ¹²³I-meta-iodobenzylguanidine (¹²³I-mIBG) scintigraphy.

In 21 RHT patients (median age 60 years), we performed ¹²³I-mIBG scintigraphy before and 6 weeks after RDN. Additionally, we assessed changes in BP (24 h day, night, and average), plasma- and urinary-catecholamines and plasma renin activity (PRA) before and after RDN. Planar scintigraphy was performed at 15 min and 4 h after ¹²³I-mIBG administration. The ratio of the mean renal (specific) counts vs. muscle (non-specific) counts represented ¹²³I-mIBG uptake. Renal ¹²³I-mIBG washout was calculated between 15 min and 4 h.

After RDN office-based systolic BP decreased from 172 to 153 mmHg (p = 0.036), while diastolic office BP (p = 0.531), mean 24 h systolic and diastolic BP (p = 0.602, p = 0.369, respectively), PRA (p = 0.409) and plasma catecholamines (p = 0.324) did not significantly change post-RDN. Following RDN, ¹²³I-mIBG renal uptake at 15 min was 3.47 (IQR 2.26-5.53) compared to 3.08 (IQR 2.79-4.95) before RDN (p = 0.289). Renal ¹²³I-mIBG washout did not change post-RDN (p = 0.230). In addition, there was no significant correlation between the number of denervations and the renal ¹²³I-mIBG parameters.

No changes were observed in renal ¹²³I-mIBG uptake or washout at 6 weeks post-RDN. These observations support incomplete renal denervation as a possible explanation for the lack of RDN efficacy.