Impact of indoxyl sulfate on progenitor cell-related neovascularization of peripheral arterial disease and post-angioplasty thrombosis of dialysis vascular access

Chih Cheng Wu, Szu Chun Hung, Ko Lin Kuo, Der Cherng Tarng*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations

Abstract

Patients with chronic kidney disease (CKD) have an increased risk of vascular disease, which is associated with considerable health care costs. Vascular disease in CKD differs clinically and pathobiologically from that in patients with normal renal function. Besides the traditional risk factors, retention of uremic toxins contributes to the pathogenesis of vascular disease in patients with CKD. Indoxyl sulfate is a protein-bound uremic toxin and is inefficiently removed by conventional dialysis. Accumulating evidence suggests that indoxyl sulfate is a vascular toxin involved in atherosclerosis, arteriosclerosis, vascular calcification and vascular repair. Clinically, indoxyl sulfate is associated with total and cardiovascular mortality in patients with CKD. Recent studies have indicated that in addition to coronary and cerebral arteries, indoxyl sulfate plays a role in peripheral artery disease (PAD) and dialysis graft thrombosis. Emerging evidence suggests that indoxyl sulfate is implicated via novel mechanisms, including progenitor cell-related neovascularization and tissue factor-related hypercoagulability. These findings raise the possibility that strategies targeting serum indoxyl sulfate may have the potential to improve the outcomes of PAD and dialysis vascular access in patients with CKD.

Original languageEnglish
Article number25
JournalToxins
Volume9
Issue number1
DOIs
StatePublished - 7 Jan 2017

Keywords

  • Chronic kidney disease
  • Dialysis vascular access
  • Indoxyl sulfate
  • Peripheral artery disease
  • Thrombosis
  • Uremic toxin

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