title: The blood pressure-lowering effect of renal denervation is inversely related to kidney function.
abstract: OBJECTIVE
  In renal denervation (RDN), a wide range in the blood pressure (BP)-lowering effect has been reported. On the basis of the current knowledge of pathophysiology, we hypothesized that the BP-lowering effect of RDN would be inversely related to kidney function. Second, we investigated whether direct and indirect variables of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS) would be related as well.
  
  
  METHODS
  Sixty-seven patients from a prospective cohort of patients treated with RDN with completed 6 months follow-up were included. Data collected during routine standardized work-up before RDN were used: 24-h urine excretion of creatinine, albumin, sodium and catecholamines, plasma creatinine, renin activity and aldosterone, ambulatory BP-monitoring and a captopril challenge test. When considered well tolerated, antihypertensive drugs were stopped before these investigations.
  
  
  RESULTS
  The BP-lowering was inversely related to estimated glomerular filtration rate (eGFR) in patients who stopped antihypertensive drugs prior to testing (ß: 0.46, P = 0.013). There was a positive relation between SBP at baseline and the BP-lowering effect of RDN (ß:-0.55 mmHg per mmHg, P < 0.001). Parameters related to the rennin-angiotensin system (aldosterone, captopril test) and the sympathetic nervous system (dipping pattern and catecholamines in urine) positively related to the BP-lowering effect of RDN.
  
  
  CONCLUSIONS
  The present explorative study shows an inverse relation between the BP-lowering effect of RDN and eGFR. Second, we found relations between variables of the RAAS and SNS with the BP-lowering effect of RDN. The data complement current concepts on pathophysiology of sympathetic hyperactivity and hypertension and may give some insight in the wide range of the effect of RDN.
authors.affiliation: aDepartment of Nephrology bDepartment of Cardiology cDepartment of Vascular Medicine dDepartment of Radiology eJulius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands.
authors.forename: Eva E
authors.initials: EE
authors.lastname: Vink
authors.forename: Willemien L
authors.initials: WL
authors.lastname: Verloop
authors.forename: Rianne B C
authors.initials: RB
authors.lastname: Bost
authors.forename: Michiel
authors.initials: M
authors.lastname: Voskuil
authors.forename: Wilko
authors.initials: W
authors.lastname: Spiering
authors.forename: Evert-Jan
authors.initials: EJ
authors.lastname: Vonken
authors.forename: Michiel L
authors.initials: ML
authors.lastname: Bots
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Blankestijn
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000378:metabolism; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000502:physiology*; D018660:Blood Pressure Monitoring, Ambulatory; D002216:Captopril / Q000378:metabolism; D003714:Denervation; D005260:Female; D006801:Humans; D006973:Hypertension / Q000601:surgery*; D007668:Kidney / Q000294:innervation* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000601:surgery
chemical_list: D000959:Antihypertensive Agents; D000450:Aldosterone; D002216:Captopril