title: Homocysteinemia correlates with plasma thiol redox status in patients with end-stage renal disease.
abstract: OBJECTIVE
  In end-stage renal disease (ESRD), hyperhomocysteinemia is a common finding associated with increased cardiovascular risk. However, the pathogenic role of homocysteine is still unclear. In vitro studies show that thiol redox status affects endothelial cell functions. We therefore investigated the possible association between homocysteinemia and plasma thiol redox status in ESRD patients.
  
  
  METHODS
  Total plasma homocysteine (Hcy), cysteine (Cys) and free thiols (SH) were measured both before and after a dialytic session in 54 ESRD patients receiving (n = 15) or not receiving (n = 39) folate supplementation, and 17 control subjects.
  
  
  RESULTS
  High predialysis levels of both Hcy and Cys were found to be negatively correlated with low SH levels both in supplemented (r = -0.680, p < 0.01 and r = -0.624, p < 0.02, respectively) and unsupplemented (r = -0.698, p < 0.001 and r = -0.445, p < 0.01, respectively) patients. Following dialysis, SH values returned to normal and the above correlations were no longer appreciable.
  
  
  CONCLUSIONS
  A strong, folate therapy-insensitive association between homocysteinemia and plasma free thiol levels was found in ESRD patients. These results support a role for oxidative stress in ESRD-related hyperhomocysteinemia and suggest the plasma thiol redox status alteration as a possible pathogenic mechanism underlying the cardiovascular toxicity of hyperhomocysteinemia in these patients.
authors.affiliation: Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy. simonetta.palleschi@iss.it
authors.forename: Simonetta
authors.initials: S
authors.lastname: Palleschi
authors.forename: Sandro
authors.initials: S
authors.lastname: De Angelis
authors.forename: Barbara
authors.initials: B
authors.lastname: Rossi
authors.forename: Loretta
authors.initials: L
authors.lastname: Diana
authors.forename: Vincenza
authors.initials: V
authors.lastname: Papa
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Severini
authors.forename: Giorgio
authors.initials: G
authors.lastname: Splendiani
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D003545:Cysteine / Q000097:blood* / Q000187:drug effects; D003956:Dialysis / Q000379:methods; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage / Q000494:pharmacology; D006710:Homocysteine / Q000097:blood* / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood* / Q000150:complications; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D018709:Statistics, Nonparametric; D013438:Sulfhydryl Compounds / Q000097:blood* / Q000378:metabolism; D014803:Vitamin B Complex / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D013438:Sulfhydryl Compounds; D006710:Homocysteine; D014803:Vitamin B Complex; D005492:Folic Acid; D003545:Cysteine