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DOI 10.1016/j.semnephrol.2004.06.009

Медицинская библиотека · Seminars in nephrology · 2004

Inflammation: cause of vascular disease and malnutrition in dialysis patients.

Kaysen George A

СтатьяПоддержка исследования: вне правительства СШАПоддержка правительства СШАПоддержка службы здравоохранения СШАОбзорПеревод пока не подготовлен

Аннотация

Inflammation occurs in response to tissue injury or the presence of foreign antigens and is important in the mobilization of specific immunologic and nonimmunologic defenses against injury. The vascular endothelium is altered to allow immune competent cells to access the interstitial space. Muscle and visceral proteins are catabolized and the amino acids are used either to supply energy or as substrates for the production of acute-phase proteins that play a role in defense. Restoration of muscle mass is impaired while inflammation is on going. Lipids are mobilized. Although serving a vital role in allowing host survival from acute injury or infection, if unimpeded, or if triggered inappropriately, the acute-phase response may instead lead to increased vascular injury and progressive loss of muscle and visceral protein pools causing malnutrition. Markers of inflammation (C reactive protein [CRP] or interleukin-6 [IL-6] levels) are associated with cardiovascular risk in the general population and in dialysis patients. Hypoalbuminemia also is associated with cardiovascular risk in dialysis patients. Although albumin is considered a marker of nutrition, changes in albumin levels are associated with increased levels of acute-phase proteins. Persistent changes in albumin levels are caused by reduced albumin synthesis associated with inflammation and not decreased normalized protein catabolic rate. The cause(s) of inflammation must be identified and treated to resolve malnutrition and reduce cardiovascular risk.

Для цитирования: Kaysen George A. Inflammation: cause of vascular disease and malnutrition in dialysis patients.. Seminars in nephrology. 2004. DOI: 10.1016/j.semnephrol.2004.06.009.

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