Polymorphism of immunomodulatory cytokine genes: implications in acute renal failure

Blood Purif. 2004;22(1):101-11. doi: 10.1159/000074930.

Abstract

Experimental studies have incriminated cytokines and other immunoregulatory molecules as important mediators of tissue injury in acute renal failure (ARF). The relative importance of genetic factors, e.g. polymorphisms involving cytokine genes, in influencing susceptibility to and severity of ARF is unknown. This review summarizes the existing experimental and clinical studies supporting the role of inflammation in ARF, and critically examines human studies that have examined polymorphism of two critical cytokine genes, tumor necrosis factor-alpha and interleukin-10, as potential determinants of susceptibility to and severity of acute infectious and inflammatory diseases. Conclusions are drawn on the application of genetic epidemiology to the field of ARF and the rationale for further research on the role of genetic markers in ARF.

Publication types

  • Review

MeSH terms

  • Acute Kidney Injury / genetics*
  • Acute Kidney Injury / physiopathology
  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Cytokines / genetics*
  • Cytokines / physiology
  • Gene Expression Regulation / drug effects
  • Glucocorticoids / pharmacology
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Inflammation / blood
  • Inflammation / genetics
  • Inflammation / physiopathology
  • Interleukin-10 / genetics
  • Ischemia / etiology
  • Kidney / blood supply
  • Polymorphism, Genetic*
  • Sepsis / blood
  • Sepsis / complications
  • Sepsis / genetics
  • Sepsis / physiopathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Glucocorticoids
  • Immunosuppressive Agents
  • Tumor Necrosis Factor-alpha
  • Interleukin-10