Cytokines, atherogenesis, and hypercatabolism in chronic kidney disease: a dreadful triad.

Abstract

The term cytokine clusters denotes a copious family of molecules and correspondent receptors implicated in numerous processes mediating health and disease. In the context of chronic kidney disease (CKD), generation and metabolism of most of these cytokines are disturbed. Available evidence suggests that cytokine imbalances contribute to the progression of common CKD complications, such as atherosclerosis, mineral-bone disease, and protein-energy wasting via pleiotropic effects. The belief that cytokine CKD research is solely represented by interleukins (IL) and tumor-necrosis factors (TNF) (mainly IL-6 and TNF-alpha) is a common misconception among nephrologists. We here explore recent findings concerning the pathophysiological role of various cytokines in uremic complications, and discuss how cytokines could be used as novel potential therapeutic targets in CKD. At the same time, we provide a brief overview of current discoveries in the main transforming growth factors and chemokines.

• Authors: Juan Jesus Carrero, Sun-Hee Park, Jonas Axelsson, Bengt Lindholm, Peter Stenvinkel
• Journal: Seminars in dialysis (Semin Dial) 2009 Jul-Aug Vol. 22 Issue 4 Pg. 381-6 ISSN: 1525-139X [Electronic] United States
• PMID: 19708986 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Cytokines

Topics

• Atherosclerosis (etiology, metabolism, pathology)
• Cytokines (physiology)
• Humans
• Kidney Diseases (etiology, metabolism, therapy)