Elsevier

Transplantation Proceedings

Volume 37, Issue 9, November 2005, Pages 3805-3807
Transplantation Proceedings

Complication
Infection
Altered metabolism: Lipids
Endothelial Dysfunction in Renal Transplant Recipients

https://doi.org/10.1016/j.transproceed.2005.09.116Get rights and content

Abstract

Endothelial dysfunction and damage are systemic processes that are recognised to play a central role in the pathogenesis of hypertension and atherosclerotic cardiovascular disease. Renal failure is associated with impaired endothelium dependent vasodilatation that is partly a consequence of increased circulating levels of asymmetric dimethyl arginine. Endothelial dysfunction persists, although it is improved, after renal transplantation. Statins appear to improve endothelial dysfunction, as does withdrawal of calcineurin inhibitors, although there is no evidence that these strategies improve patient or graft survival. The situation in transplant recipients is complicated by the fact that endothelial dysfunction (within the graft vasculature) may be a separate process contributing to chronic allograft nephropathy and to circulating levels of endothelial cells and their components, thus limiting the utility of circulating markers of endothelial damage in this population.

Section snippets

Endothelial dysfunction: definitions, mechanisms, and measurement

Under normal circumstances, the main role of the endothelium is to facilitate vasodilatation and inhibit platelet adhesion through the production of nitric oxide (NO). Reduced production of NO is the predominant component of endothelial dysfunction, leading to enhanced vasoconstriction and platelet adhesion (and activation). The loss of vasodilatation contributes to development of hypertension. However, there are additional factors that contribute to the measurement of endothelial dysfunction.

Underlying mechanisms and interventions

Two main factors contribute to endothelial dysfunction and the impaired release of NO in response to agonists like carbachol. The first is the production of superoxide that reacts with NO to produce peroxynitrite. Superoxide and other free radicals are a result of oxidative stress and are dependent on factors such as cigarette smoking, vasoactive compounds (eg, angiotensin II and endothelin), and lipids (eg, oxidised low density lipoprotein). This pathway may explain some of the benefits of,

Intervention

If endothelial dysfunction is central to the development of atherosclerotic CVD, the question arises of how to reverse this abnormality. There are no interventions that independently reverse ED, although interventions that reduce CV risk in other populations are associated with improved endothelial function. These include lifestyle measures, such as weight loss, exercise, and smoking cessation. The reduction of homocysteine levels by the use of folic acid is associated with improved ED in the

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