Now Available for Public Comment: Notice of Proposed Rulemaking (NPRM) for FDAAA 801 and NIH Draft Reporting Policy for NIH-Funded Trials

Renal Nerve Ablation in Chronic Kidney Disease Patients

This study is currently recruiting participants. (see Contacts and Locations)
Verified January 2013 by University of Erlangen-Nürnberg Medical School
Sponsor:
Information provided by (Responsible Party):
University of Erlangen-Nürnberg Medical School
ClinicalTrials.gov Identifier:
NCT01442883
First received: September 22, 2011
Last updated: January 18, 2013
Last verified: January 2013

September 22, 2011
January 18, 2013
November 2010
December 2013   (final data collection date for primary outcome measure)
  • office BP [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    Change in office blood pressure from baseline to 6 months post-renal nerve ablation
  • 24-h ABPM [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    Change in 24 hour ambulatory blood pressure (ABPM) from baseline to 6 months post-renal nerve ablation
  • Magnetic resonance imaging (MRI) [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    • change in total sodium content measured by MRI from baseline to 6 months post-renal nerve ablation
    • change in renal perfusion measured by MRI spin labelling technique from baseline to 6 months post-renal nerve ablation
  • Albuminuria [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    Change in urinary albumin/creatinine ratio from baseline to 6 months post renal nerve ablation (spot urine)
  • local RAS activity [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    Change in urinary angiotensinogen concentration from the morning spot urine from baseline to 6 months post-renal nerve ablation
  • systemic RAS activity [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    • change in sodium, potassium and creatinine from baseline to 6 months post-renal nerve ablation
    • change in aldosterone excretion from baseline to 6 months post-renal nerve ablation
    • change in sodium / potassium ratio from baseline to 6 months post-renal nerve ablation
    • change in plasma renin activity and angiotensin II concentration at least 30 minutes of rest in a supine position and immediately after standing from baseline to 6 months post-renal nerve ablation
  • vascular structure and function of large and small arteries [ Time Frame: baseline, 6 months ] [ Designated as safety issue: No ]
    • change in flow-mediated vasodilation (FMD) from baseline to 6 months post-renal nerve ablation
    • change in scanning laser Doppler flowmetry (SLDF) from baseline to 6 months post-renal nerve ablation
    • change in pulse wave analysis (PWA) from baseline to 6 months post-renal nerve ablation
    • change in pulse wave velocity from (PWV) baseline to 6 months post-renal nerve ablation
    • change in urinary albumine creatinine ratio (UACR) of the morning spot urine sample from baseline to 6 months post-renal nerve ablation
Same as current
Complete list of historical versions of study NCT01442883 on ClinicalTrials.gov Archive Site
  • BP [ Time Frame: 1 and 12 months ] [ Designated as safety issue: No ]
    • change in office blood pressure from baseline to 1 and 12 months post-renal nerve ablation
    • change in 24 hour ambulatory blood pressure from baseline to 1 and 12 months post-renal nerve ablation
  • local RAS activity [ Time Frame: 1 day and 1 months ] [ Designated as safety issue: No ]
    Change in urinary angiotensinogen concentration from the morning spot urine from baseline to 1 day and 1 months post-renal nerve ablation
  • systemic RAS activity [ Time Frame: 1 day and 1 months ] [ Designated as safety issue: No ]
    • change in sodium, potassium and creatinine from baseline to 1 day and 1 months post-renal nerve ablation
    • change in albuminuria from baseline to 1 and 12 months post-renal nerve ablation
    • change in aldosterone excretion from baseline to 1 day and 1 months post-renal nerve ablation
    • change in sodium / potassium ratio from baseline to 1 day and 1 months post-renal nerve ablation
    • change in plasma renin activity and angiotensin II concentration at least 30 minutes of rest in a supine position and immediately after standing from baseline to 1 day and 1 months post-renal nerve ablation
  • vascular structure and function of large and small arteries [ Time Frame: 12 months ] [ Designated as safety issue: No ]
    • change in flow-mediated vasodilation (FMD) from baseline to 12 months post-renal nerve ablation
    • change in scanning laser Doppler flowmetry (SLDF) from baseline to 12 months post-renal nerve ablation
    • change in pulse wave analysis (PWA) from baseline to 12 months post-renal nerve ablation
    • change in pulse wave velocity from (PWV) baseline to 12 months post-renal nerve ablation
    • change in urinary albumine creatinine ratio (UACR) of the morning spot urine sample from baseline to 12 months post-renal nerve ablation
  • MRI [ Time Frame: 1 day, 1 and 12 months ] [ Designated as safety issue: No ]
    • change in total sodium content measured by MRI from baseline to 12 months post-renal nerve ablation
    • change in renal perfusion measured by MRI spin labelling technique from baseline to 1 day and 1 months post-renal nerve ablation
  • BP [ Time Frame: 1 and 12 months ] [ Designated as safety issue: No ]
    • change in office blood pressure from baseline to 1 and 12 months post-renal nerve ablation
    • change in 24 hour ambulatory blood pressure from baseline to 1 and 12 months post-renal nerve ablation
  • local RAS activity [ Time Frame: 1 day and 1 months ] [ Designated as safety issue: No ]
    Change in urinary angiotensinogen concentration from the morning spot urine from baseline to 1 day and 1 months post-renal nerve ablation
  • systemic RAS activity [ Time Frame: 1 day and 1 months ] [ Designated as safety issue: No ]
    • change in sodium, potassium and creatinine from baseline to 1 day and 1 months post-renal nerve ablation
    • change in albuminuria from baseline to 1 and 12 months post-renal nerve ablation
    • change in aldosterone excretion from baseline to 1 day and 1 months post-renal nerve ablation
    • change in sodium / potassium ratio from baseline to 1 day and 1 months post-renal nerve ablation
    • change in plasma renin activity and angiotensin II concentration at least 30 minutes of rest in a supine position and immediately after standing from baseline to 1 day and 1 months post-renal nerve ablation
  • vascular structure and function of large and small arteries [ Time Frame: 12 months ] [ Designated as safety issue: No ]
    • change in flow-mediated vasodilation (FMD) from baseline to 12 months post-renal nerve ablation
    • change in scanning laser Doppler flowmetry (SLDF) from baseline to 12 months post-renal nerve ablation
    • change in pulse wave analysis (PWA) from baseline to 12 months post-renal nerve ablation
    • change in pulse wave velocity from (PWV) baseline to 12 months post-renal nerve ablation
    • change in urinary albumine creatinine ratio (UACR) of the morning spot urine sample from baseline to 12 months post-renal nerve ablation
  • MRI [ Time Frame: 1 day, 1 and 12 months ] [ Designated as safety issue: No ]
    • change in total sodium content mesasured by MRI from baseline to 12 months post-renal nerve ablation
    • change in renal perfusion measured by MRI spin labelling technique from baseline to 1 day and 1 months post-renal nerve ablation
Not Provided
Not Provided
 
Renal Nerve Ablation in Chronic Kidney Disease Patients
Understanding the Mechanisms of Progressive Decrease in Blood Pressure After Renal Nerve Ablation

In patients with treatment resistent hypertension renal nerve ablation emerged as an effective interventional approach of treating hypertensive disease with a progressively increasing fall in blood pressure. Decreased activity of the sympathetic nervous system is one of the major underlying pathogenetic mechanism of the fall in blood pressure but the precise mechanisms that causes the fall in blood pressure in the short-term and, in particular, long-term remains elusive. The objective of the study is to understand the pathogenetic mechanisms of renal denervation beyond the reduced activity of the sympathetic nervous system. In 100 hypertensive patients most advanced technology will be applied, before and repeatedly after renal denervation, throughout the follow-up period of 1 year. Systemic activity of the renin angiotensin aldosterone system, renal perfusion (by MRI spin labelling technique), local activity of the renin angiotensin system in the kidney (urinary angiotensinogen concentrations), sodium excretion and total sodium content (23 Na-MRI technique) and vascular remodelling of small (retinal arterioles 50 - 150 µm) and large arteries (carotid - femoral pulse wave velocity and augmentation index, both measured over 24 hours) will be assessed. Identification of the pathogenetic mechanisms involved in the fall in blood pressure after renal denervation may help to identify those hypertensive patients that profit most from renal nerve ablation in terms of blood pressure reduction.

The investigators propose the following hypotheses why a progressive decrease in blood pressure happens, in addition to the decreased activity of the central nervous system, after renal nerve ablation:

Short term effects:

A)Preservation of renal function and perfusion B)Reduction of local RAS activity in the kidney C)Exaggerated sodium excretion immediately after renal nerve ablation

Long term effects:

D)Decrease of total sodium content after 6 and 12 months. E)Improvement of vascular wall properties after 6 and 12 months

In patients with treatment resistent hypertension renal nerve ablation emerged as an effective interventional approach of treating hypertensive disease with a progressively increasing fall in blood pressure. Decreased activity of the sympathetic nervous system is one of the major underlying pathogenetic mechanism of the fall in blood pressure but the precise mechanisms that causes the fall in blood pressure in the short-term and, in particular, long-term remains elusive. The objective of the study is to understand the pathogenetic mechanisms of renal denervation beyond the reduced activity of the sympathetic nervous system. In 100 hypertensive patients most advanced technology will be applied, before and repeatedly after renal denervation, throughout the follow-up period of 1 year. Systemic activity of the renin angiotensin aldosterone system, renal perfusion (by MRI spin labelling technique), local activity of the renin angiotensin system in the kidney (urinary angiotensinogen concentrations), sodium excretion and total sodium content (23 Na-MRI technique) and vascular remodelling of small (retinal arterioles 50 - 150 µm) and large arteries (carotid - femoral pulse wave velocity and augmentation index, both measured over 24 hours) will be assessed. Identification of the pathogenetic mechanisms involved in the fall in blood pressure after renal denervation may help to identify those hypertensive patients that profit most from renal nerve ablation in terms of blood pressure reduction.

Observational
Observational Model: Cohort
Time Perspective: Prospective
Not Provided
Not Provided
Non-Probability Sample

treatment resistant hypertensive adults with chronic kidney disease 3 - 5

  • Hypertension
  • Chronic Kidney Disease
Device: Simplicity Catheter
percutaneous selective renal sympathetic nerve ablation with the use of the Simplicity Catheter system
treatment resistant hypertensives with CKD 3-5
Intervention: Device: Simplicity Catheter
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
100
December 2013
December 2013   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • treatment resistant hypertension
  • chronic kidney disease 3 - 5
  • male of female aged over 18 years
  • written informed consent
  • agreement to attend all study visits as planned in the protocol

Exclusion Criteria:

  • any contraindications for MRI
  • claustrophobia
  • strabismus
  • severe ocular diseases
  • history of epilepsia
Both
18 Years to 85 Years
No
Contact: Christian Ott, MD +49-9131-85 ext 36245 christian.ott@uk-erlangen.de
Germany
 
NCT01442883
RNA-CKD3-5
No
University of Erlangen-Nürnberg Medical School
University of Erlangen-Nürnberg Medical School
Not Provided
Principal Investigator: Roland E Schmieder, MD University of Erlangen-Nürnberg, Germany
University of Erlangen-Nürnberg Medical School
January 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP