A nexus of progression of chronic kidney disease: charcoal, tryptophan and profibrotic cytokines

Blood Purif. 2006;24(1):143-8. doi: 10.1159/000089451.


Fibrosis plays a role in the pathogenesis of progressive chronic kidney disease (CKD). The inhibition of the renin-angiotensin system, which promotes fibrosis, has become the standard of care in the treatment of patients with CKD. A novel charcoal compound, AST-120, has been used for over a decade in Japan to prevent progression of CKD. It is thought that the oral administration of AST-120 blocks the intestinal absorption of tryptophan-derived indole. This prevents the hepatic conversion of indole to indoxyl sulfate (IS). IS has been shown to stimulate the production of profibrotic cytokines such as transforming growth factor-beta. AST-120 lowers IS in a dose dependent fashion and does not change the creatinine appearance rate in the urine. Enteric capsules containing Bifidobacterium longum have been shown to prevent progression of CKD in a preliminary study. These findings suggest that prospective clinical trials be undertaken to determine if these other potential methods of inhibiting fibrosis are useful in slowing progressive CKD.

Publication types

  • Randomized Controlled Trial

MeSH terms

  • Administration, Oral
  • Adult
  • Aged
  • Carbon / administration & dosage*
  • Cytokines / metabolism
  • Endpoint Determination
  • Female
  • Fibrosis / blood
  • Fibrosis / drug therapy
  • Fibrosis / etiology
  • Humans
  • Indican / blood
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Failure, Chronic / blood
  • Kidney Failure, Chronic / complications
  • Kidney Failure, Chronic / drug therapy*
  • Kidney Failure, Chronic / pathology
  • Male
  • Middle Aged
  • Oxides / administration & dosage*
  • Tryptophan / metabolism


  • Cytokines
  • Oxides
  • Carbon
  • Tryptophan
  • AST 120
  • Indican