The role of inflammation in the anaemia of end-stage renal disease

Nephrol Dial Transplant. 2001;16 Suppl 7:36-40. doi: 10.1093/ndt/16.suppl_7.36.


Chronic inflammation is a common feature of end-stage renal disease (ESRD) that is gaining increasing attention as a major cause of morbidity and mortality. It is well established that ESRD per se carries a heightened risk of inflammatory disorders and other co-morbid conditions, but it should also be pointed out that dialysis treatment per se can bring additional risk factors for inflammation, such as impure dialysate or bio-incompatible membranes. Inflammation has recently been associated with atherosclerosis and malnutrition in ESRD, and this link has led to the development of the malnutrition, inflammation, atherosclerosis (MIA) hypothesis. This describes a syndrome whereby raised levels of pro-inflammatory cytokines (such as IL-1, IL-6 and TNF-alpha) are a common link between malnutrition, inflammation and atherosclerosis. Also, anaemia appears to be an important element linking elevated cytokine levels with poor patient outcomes. Several mechanisms for cytokine-induced anaemia have been proposed, including intestinal bleeding, impaired iron metabolism and suppression of bone marrow erythropoiesis and erythropoietin production. These effects suggest that pro-inflammatory cytokines may also be an important cause of lack of response to recombinant human erythropoietin (rh-Epo) therapy. In the light of this putative role of pro-inflammatory cytokines, anti-cytokine agents may prove useful to optimize efficacy of rh-Epo in anaemic chronic renal failure patients. Other potential therapeutic strategies include minimizing exposure to causes of inflammation from various co-morbid conditions, such as persistent infections and chronic heart failure.

Publication types

  • Review

MeSH terms

  • Anemia / drug therapy
  • Anemia / etiology*
  • Anemia / physiopathology*
  • Cytokines / physiology
  • Humans
  • Inflammation / physiopathology*
  • Inflammation Mediators / physiology
  • Kidney Failure, Chronic / complications*
  • Kidney Failure, Chronic / physiopathology
  • Models, Biological


  • Cytokines
  • Inflammation Mediators