Do Xanthine Oxidase Inhibitors Reduce Both Left Ventricular Hypertrophy and Endothelial Dysfunction in Cardiovascular Patients With Renal Dysfunction? - Tabular View

Tracking Information

First Received Date ^ICMJE

May 29, 2008

Last Updated Date

July 10, 2008

Start Date ^ICMJE

January 2008

Estimated Primary Completion Date

November 2009 (final data collection date for primary outcome measure)

Current Primary Outcome Measures ^ICMJE

Primary objective is to see if Allopurinol reduces left ventricular hypertrophy (LVH) in this group of CKD patients [ Time Frame: 9 months ] [ Designated as safety issue: No ]

Original Primary Outcome Measures ^ICMJE

Same as current

Change History

Complete list of historical versions of study NCT00688480 on ClinicalTrials.gov Archive Site

Current Secondary Outcome Measures ^ICMJE

Secondary objective is to see if Allopurinol reduces endothelial dysfunction in this group of CKD patients [ Time Frame: 9 months ] [ Designated as safety issue: No ]

Original Secondary Outcome Measures ^ICMJE

Same as current

Descriptive Information

Brief Title ^ICMJE

Do Xanthine Oxidase Inhibitors Reduce Both Left Ventricular Hypertrophy and Endothelial Dysfunction in Cardiovascular Patients With Renal Dysfunction?

Official Title ^ICMJE

Do Xanthine Oxidase Inhibitors Reduce Both Left Ventricular Hypertrophy and Endothelial Dysfunction in Cardiovascular Patients With Renal Dysfunction?

Brief Summary

Cardiovascular related disease is the main cause of death in patients with kidney disease, and "oxidative stress" is thought to be a major contributor by promoting thickening of the heart muscle and stiffening of the arteries. Allopurinol, a drug used safely in the treatment of gout for many years, has been found to dramatically reduce "oxidative stress". It is therefore hoped that it also reduce the thickened heart muscle and stiffened arteries. If it did, it is likely to reduce the appallingly high cardiac death rate in this group of kidney disease patients.

Detailed Description

Study Phase

Phase IV

Study Type ^ICMJE

Interventional

Study Design ^ICMJE

Treatment, Randomized, Double Blind (Subject, Investigator), Placebo Control, Parallel Assignment, Efficacy Study

Condition ^ICMJE

Kidney Disease
Left Ventricular Hypertrophy

Intervention ^ICMJE

Drug: Placebo
Drug: Allopurinol

Study Arms / Comparison Groups

Placebo Comparator: CKD Stage 3 (estimated GFR 30 - 60 ml/min/1.73m2), Echo LVH

Publications *

* Includes publications given by the data provider as well as publications identified by National Clinical Trials Identifier (NCT ID) in Medline.

Recruitment Information

Recruitment Status ^ICMJE

Recruiting

Estimated Enrollment ^ICMJE

Estimated Completion Date

November 2009

Estimated Primary Completion Date

November 2009 (final data collection date for primary outcome measure)

Eligibility Criteria ^ICMJE

Inclusion Criteria:

CKD stage 3
Echo LVH

Exclusion Criteria:

Known heart failure
Patients already on Allopurinol
Patients with gout
Patients with hepatic disease
Contraindications to MRI, including severe claustrophobia
Current immunosuppressive therapy, chlorpropamide, theophylline, 6- mercaptopurine
Malignancy or other life threatening disease
Pregnancy or lactating women
Patients unable to provide written consent

Gender

Both

Ages

18 Years and older

Accepts Healthy Volunteers

Yes

Contacts ^ICMJE

Contact: Michelle Kao, MBChB, MRCP	44-138-266-0111 ext 33452	m.kao@dundee.ac.uk
Contact: Allan Struthers, MBChB, MRCP, MD, FRCP	44-138-263-2180	a.d.struthers@dundee.ac.uk

Location Countries ^ICMJE

United Kingdom

Administrative Information

NCT ID ^ICMJE

NCT00688480

Responsible Party

Professor Allan Struthers, University of Dundee

Study ID Numbers ^ICMJE

MK001

Study Sponsor ^ICMJE

University of Dundee

Collaborators ^ICMJE

Investigators ^ICMJE

Principal Investigator:

Allan D Struthers, BSc, MD, FRCP, FESC

University of Dundee

Information Provided By

University of Dundee

Verification Date

May 2008

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