The effects of renal denervation on adipokines and pro-inflammatory status in patients with resistant arterial hypertension associated with type 2 diabetes mellitus

Introduction. Pro-inflammatory biomarkers and adipokines are involved in the regulation of blood pressure (BP) and atherogenesis and are also associated with the sympathetic nervous system. Patients with resistant hypertension (RHTN) associated with type 2 diabetes mellitus (T2DM) are characterized by high sympathetic activity, adipokine imbalance, and pro-inflammatory activity. Moreover, renal denervation (RDN) is accompanied by a decrease in sympathetic tone. Aim. To evaluate the effect of RDN on the adipokine profile and the levels of pro-inflammatory markers in patients with RHTN associated with T2DM. Material and Methods. Forty-three patients with RHTN associated with T2DM were included in the single-arm prospective interventional study. Detailed protocols are available on ClinicalTrial.gov, numbers NCT01499810 and NCT02667912. The measurements of body mass index (BMI), waist circumference (WC), office BP, 24-hour ambulatory BP, lab tests (serum concentrations of hsCRP, TNF-α, adiponectin, leptin, resistin, and IL-6) were performed at baseline and at 6and 12-month follow-ups. The one-year follow-up period of observation was completed with 40 patients. Results. Significant and consistent reductions of BP, TNF-α, and hsCRP were observed 12 months after RDN. Additionally, there were substantial increases in both adiponectin and leptin levels. The change in TNF-α was directly related to the reduction in variability of systolic BP, whereas the changes in hsCRP, adiponectin and leptin levels had no relations with BP reduction. The BMI, WC, and resistin and IL-6 levels did not change after RDN. Conclusions. This study demonstrated the ability of RDN to improve the adipokine profile and to reduce the activity of subclinical inflammation in patients with RHTN associated with T2DM. Increased adiponectin and leptin as well as reduced TNF-α and hsCRP production may contribute to BP reduction via metabolic and neuro-hormonal pathways.