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| Sponsors and Collaborators: |
St George's, University of London British Heart Foundation St. George's Hospital Charitable Foundation |
|---|---|
| Information provided by: | St George's, University of London |
| ClinicalTrials.gov Identifier: | NCT00141622 |
Purpose
Heart disease and stroke, known as cardiovascular disease, are major causes of death in people with chronic kidney disease. Abnormalities of a metabolic pathway called the “L-arginine-nitric oxide” pathway are thought to be particularly important in these people, and previous research in animals has suggested that sodium (salt) affects part of this metabolic pathway. The purpose of our research is to study the effects of sodium intake on the “L-arginine-nitric oxide” pathway, and on blood vessel function, in patients with kidney disease.
| Condition | Intervention |
|---|---|
|
Kidney Failure, Chronic |
Drug: Slow sodium |
| Study Type: | Interventional |
| Study Design: | Prevention, Randomized, Double-Blind, Placebo Control, Crossover Assignment |
| Official Title: | Does Sodium Affect Endothelial Function in Individuals With Chronic Kidney Disease? |
| Estimated Enrollment: | 50 |
| Study Start Date: | April 2005 |
| Estimated Study Completion Date: | October 2006 |
Chronic kidney disease (CKD) is associated with abnormalities of endothelial function (EF) and nitric oxide (NO) synthesis, and it is proposed that the endogenous NO synthase inhibitor asymmetrical dimethylarginine (ADMA) plays a central role. In man ADMA is largely metabolized by dimethylarginine dimethylaminohydrolase (DDAH), with some renal excretion occurring. Sodium inhibits DDAH expression in experimental animals and, given that CKD is frequently characterized by sodium retention, it would be interesting to study the effects of sodium loading on DDAH activity/expression, ADMA levels and EF in CKD patients.
To answer these questions, we have designed a double-blind cross-over study employing Slow Sodium (150 mmol/day) and placebo for seven days in individuals with mild-to-moderate CKD. Changes in the ratio of urinary ADMA to dimethylamine (DMA, an ADMA metabolite) will be used as an marker of DDAH activity/expression. ADMA will be measured by ELISA, DMA by high performance liquid chromatography, and EF by venous occlusion plethysmography.
We propose to test the following hypothesis; that in subjects with mild-to-moderate CKD under conditions of high sodium intake, as compared to low-normal sodium intake:
(i) The ratio [ADMA]urine:[DMA]urine is increased (ii) [ADMA]plasma is increased (iii) Endothelium-dependent vasodilatation is reduced
Eligibility| Ages Eligible for Study: | 18 Years to 75 Years |
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | No |
Inclusion Criteria:
Exclusion Criteria:
Contacts and Locations| United Kingdom | |
| Blood Pressure Unit, Department of Cardiac & Vascular Sciences, SGUL | |
| LONDON, United Kingdom, SW17 0RE | |
| Principal Investigator: | Timothy WR Doulton, BSc MRCP | SGUL |
More Information
| Study ID Numbers: | LREC 04/Q0803/181 |
| Study First Received: | August 31, 2005 |
| Last Updated: | May 14, 2007 |
| ClinicalTrials.gov Identifier: | NCT00141622 |
| Health Authority: | United Kingdom: Research Ethics Committee |
|
Endothelial dysfunction ADMA DDAH Sodium |
|
Renal Insufficiency Urologic Diseases Renal Insufficiency, Chronic |
Kidney Failure, Chronic Kidney Diseases Kidney Failure |
