title: Effects of vitamin supplementation on microcirculatory disturbance in hemodialysis patients without peripheral arterial disease.
abstract: OBJECTIVE
  Dysfunctional endothelium caused by oxidative stress is thought to play a role in pathogenesis of a variety of conditions including atherosclerosis. We investigated whether a microcirculatory disturbance in hemodialysis (HD) patients was associated with increased oxidative stress and endothelial injury.
  
  
  METHODS
  Transcutaneous oxygen tension (TcPO2) on the dorsum of the foot at rest was measured as a marker of microcirculation in 33 patients undergoing HD without clinical manifestations of peripheral arterial disease and 20 healthy controls. Furthermore, in order to examine whether TcPO2 was affected by antioxidants, oral supplementation with a combination of vitamin C (200 mg daily) and vitamin E (600 mg daily) was administered for 6 months to 8 patients with microcirculatory disturbance (TcPO2 values of 50 mmHg or less). Serum biochemical parameters including vitamins were also measured.
  
  
  RESULTS
  Mean TcPO2 value was significantly lower in HD patients than in control subjects (47.9 +/- 13.5 mmHg versus 62.4 +/- 11.9 mmHg, p < 0.001). After vitamin supplementation, TcPO2 values remarkably increased (40.6 +/- 10.0 mmHg versus 57.4 +/- 6.5 mmHg, p < 0.005). Serum vitamin C and vitamin E levels increased significantly as well, while serum levels of thrombomodulin, a marker of endothelial injury, and thiobarbituric acid reactants, a marker of lipid peroxidation, were significantly decreased in comparison with those before supplementation.
  
  
  CONCLUSIONS
  Our results suggest that the microcirculatory disturbance in HD patients seems to be associated with endothelial damage caused by oxidative stress. Combined supplementation with vitamin C and vitamin E may be of clinical benefit in improving the cutaneous microcirculation by reducing oxidative stress.
authors.affiliation: Department of Dialysis Therapy, Social Insurance Chukyo Hospital, Nagoya, Japan. ca8m-stu@asahi-net.or.jp
authors.forename: M
authors.initials: M
authors.lastname: Sato
authors.forename: Y
authors.initials: Y
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Morita
authors.forename: H
authors.initials: H
authors.lastname: Takemura
authors.forename: K
authors.initials: K
authors.lastname: Shimoi
authors.forename: I
authors.initials: I
authors.lastname: Amano
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D001785:Blood Gas Monitoring, Transcutaneous; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D005528:Foot; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D015227:Lipid Peroxidation; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology; D016491:Peripheral Vascular Diseases / Q000503:physiopathology; D006435:Renal Dialysis; D012867:Skin / Q000098:blood supply*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D018180:Thrombomodulin / Q000032:analysis; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D018180:Thrombomodulin; D014810:Vitamin E; D001205:Ascorbic Acid