title: The Effects of Renal Denervation on Renal Hemodynamics and Renal Vasculature in a Porcine Model.
abstract: BACKGROUND
  Recently, the efficacy of renal denervation (RDN) has been debated. It is discussed whether RDN is able to adequately target the renal nerves.
  
  
  OBJECTIVE
  We aimed to investigate how effective RDN was by means of functional hemodynamic measurements and nerve damage on histology.
  
  
  RESULTS
  We performed hemodynamic measurements in both renal arteries of healthy pigs using a Doppler flow and pressure wire. Subsequently unilateral denervation was performed, followed by repeated bilateral hemodynamic measurements. Pigs were terminated directly after RDN or were followed for 3 weeks or 3 months after the procedure. After termination, both treated and control arteries were prepared for histology to evaluate vascular damage and nerve damage. Directly after RDN, resting renal blood flow tended to increase by 29±67% (P = 0.01). In contrast, renal resistance reserve increased from 1.74 (1.28) to 1.88 (1.17) (P = 0.02) during follow-up. Vascular histopathology showed that most nerves around the treated arteries were located outside the lesion areas (8±7 out of 55±25 (14%) nerves per pig were observed within a lesion area). Subsequently, a correlation was noted between a more impaired adventitia and a reduction in renal resistance reserve (β: -0.33; P = 0.05) at three weeks of follow-up.
  
  
  CONCLUSIONS
  Only a small minority of renal nerves was targeted after RDN. Furthermore, more severe adventitial damage was related to a reduction in renal resistance in the treated arteries at follow-up. These hemodynamic and histological observations may indicate that RDN did not sufficiently target the renal nerves. Potentially, this may explain the significant spread in the response after RDN.
authors.affiliation: Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Willemien L
authors.initials: WL
authors.lastname: Verloop
authors.affiliation: Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Lisette E G
authors.initials: LE
authors.lastname: Hubens
authors.affiliation: Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Wilko
authors.initials: W
authors.lastname: Spiering
authors.affiliation: Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Pieter A
authors.initials: PA
authors.lastname: Doevendans
authors.affiliation: Department of Pathology, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Roel
authors.initials: R
authors.lastname: Goldschmeding
authors.affiliation: Department of Anatomy, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Ronald L A W
authors.initials: RL
authors.lastname: Bleys
authors.affiliation: Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
authors.forename: Michiel
authors.initials: M
authors.lastname: Voskuil
mesh_terms: D000818:Animals; D003714:Denervation; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation* / Q000503:physiopathology; D011312:Pressure; D012077:Renal Artery / Q000294:innervation* / Q000503:physiopathology; D012079:Renal Circulation / Q000502:physiology; D013552:Swine; D013564:Sympathetic Nervous System / Q000503:physiopathology