학술논문

Protecting the endothelium: A new focus for management of chronic kidney disease
Document Type
Author abstract
Disease/Disorder overview
Source
Hemodialysis International. Jan, 2006, Vol. 10 Issue 1, p42, 7 p.
Subject
Kidney diseases -- Development and progression
Language
English
ISSN
1492-7535
Abstract
To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1542-4758.2006.01173.x Byline: Jose A. DIAZ-BUXO (1), H. Feidhlim WOODS (2) Keywords: Chronic kidney disease; cardiovascular disease; hemodialysis; inflammation; oxidative stress; endothelial dysfunction Abstract: Abstract It is being increasingly recognized that cardiovascular disease (CVD) and its complications are the most important cause of morbidity and mortality in patients with chronic kidney disease (CKD) and dialysis patients. If outcomes for these patients are to be improved, therapeutic strategies at all stages of CKD will have to target the etiologies and mechanisms that lead to CVD. In this review, we focus on the central role of endothelial dysfunction as the critical precursor of CVD. We argue that a better understanding of endothelial dysfunction by nephrologists and dialysis physicians is necessary if there is to be success in limiting the CVD epidemic that kills and maims our patients. The extensive studies to explain the high prevalence of vascular disease in patients with CKD have shown the close relationship among endothelial dysfunction, inflammation, and atherosclerosis. The pathogenesis starts with endothelial cell injury from any of many possible causes, and strategies to reduce the burden of CVD in uremic and dialysis patients must be directed at restoring normal endothelial function or, at the least, preventing aggravation of endothelial damage. At the center of the exploration of endothelial dysfunction and atherosclerosis are oxidative stress and inflammation. Of these, which is the chicken and which is the egg is unknown, but in the setting of uremia, endothelial injury because of free radical, oxidative stress is likely to precede inflammation. The issues raised here are highly complex and most renal practitioners may not have been adequately exposed to the background research underlying current thinking of the pathogenesis of vascular disease. Clearly, progress in management of CVD in patients with CKD will require collaboration with experts in the research and treatment of vascular disease. Nephrologists seeking optimum outcomes for patients with CKD will need to become "endotheliologists" or, at the least, subscribe to a mission "to protect the endothelium." Author Affiliation: (1)Fresenius Medical Care North America, Lexington, Massachusetts, USA (2)Fresenius Medical Care Asia Pacific, Hong Kong Article History: Manuscript received March 2005; revised October 2005. Article note: Correspondence to: J. A. Diaz-Buxo, MD, FACP, 1001 Morehead Square Drive, Suite 470, Charlotte, NC 28203, U.S.A. E-mail: jose.diaz-buxo@fmc-na.com