Adipose tissue and inflammation in chronic kidney disease

Contrib Nephrol. 2006;151:165-174. doi: 10.1159/000095327.


Cardiovascular disease remains a major cause of morbidity and mortality in end-stage renal disease patients. As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of cardiovascular disease in this high-risk population, inflammation (interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor. Recent studies show that the adipose tissue is a complex organ with functions far beyond the mere storage of energy. Indeed, it has been shown that fat tissue secretes a number of adipokines including leptin, adiponectin and visfatin, as well as a cytokines (here defined as signaling proteins mainly secreted by other cells present in adipose tissue, but sometimes also to a lesser degree by adipocytes per se), such as resistin, tumor-necrosis factor-alpha and interleukin-6. Adipokine serum levels are markedly elevated in chronic kidney disease, probably due to decreased renal excretion. Evidence suggests that they may have pro-inflammatory effects as well as contribute to metabolic derangements. Much research is thus still needed to elucidate the likely complex interactions between different fat tissue depots, muscle tissue and its' effects on inflammation, vascular health and outcome in this high-risk population.

Publication types

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

MeSH terms

  • Adipose Tissue / immunology*
  • Adipose Tissue / physiopathology
  • Cardiovascular Diseases / immunology*
  • Cardiovascular Diseases / physiopathology
  • Humans
  • Inflammation / immunology*
  • Inflammation / physiopathology
  • Kidney Failure, Chronic / immunology*
  • Kidney Failure, Chronic / physiopathology