Recent insights in inflammation-associated wasting in patients with chronic kidney disease

Contrib Nephrol. 2011;171:120-126. doi: 10.1159/000327228. Epub 2011 May 23.

Abstract

In patients with end-stage renal disease (ESRD), inflammation, and protein energy wasting (PEW) are two highly prevalent and interconnected entities, jointly exerting a deleterious effect on multiple other ESRD-specific pathological processes and eventually on patient outcome. With respect to the pathophysiology underlying this strong association, knowledge has been actively expanded over the past few years. As such, it is nowadays recognized that inflammation acts via direct, as well as indirect, pathways in its contribution to PEW. Directly, inflammation causes alterations in amino acid utilization, translating into increased catabolism and decreased anabolism of muscle tissue. Indirectly, inflammation may act via altered ghrelin and adipokine metabolism, adipose tissue distribution, and pathological neuroendocrine signaling, as well as coexistent depression in inducing anorexia and PEW. In addition, two relatively new inflammatory markers (pentraxin-3 and TNF-like weak inducer of apoptosis) have gained attention with respect to their roles in this specific context. The current review deals with recent updates in the literature on the aforementioned pathways connecting inflammation to PEW and subsequent mortality.

Publication types

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

MeSH terms

  • C-Reactive Protein / physiology
  • Chronic Disease
  • Cytokine TWEAK
  • Humans
  • Inflammation / complications*
  • Kidney Diseases / complications*
  • Serum Amyloid P-Component / physiology
  • Tumor Necrosis Factors / physiology
  • Wasting Syndrome / etiology*

Substances

  • Cytokine TWEAK
  • Serum Amyloid P-Component
  • TNFSF12 protein, human
  • Tumor Necrosis Factors
  • PTX3 protein
  • C-Reactive Protein