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

Semin Dial. Jul-Aug 2009;22(4):381-6. doi: 10.1111/j.1525-139X.2009.00585.x.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Atherosclerosis / etiology*
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology
  • Cytokines / physiology*
  • Humans
  • Kidney Diseases / etiology*
  • Kidney Diseases / metabolism*
  • Kidney Diseases / therapy

Substances

  • Cytokines