title: Increasing plasma homocysteine during follow-up in heart transplant recipients: effects of folate and renal function.
abstract: BACKGROUND
  Hyperhomocysteinemia is a common finding in heart transplant recipients and may represent a risk factor for graft failure. However, the time-course, determinants and effects of medical therapy on total homocysteine plasma levels after heart transplantation remain undetermined. The aim of this study was to prospectively analyze 1) the time-course of total homocysteine in heart transplant recipients; 2) the effects of folate supplements and cyclosporine A on total homocysteine; 3) the relation among renal function, serum vitamin levels, and total homocysteine.
  
  
  METHODS
  Fifty-two heart transplant recipients consecutively evaluated for routine follow-up during 1998 were included in the study (mean age 54 +/- 12 years; 28% female). Among the 52 patients, 10 patients were treated with folate for the entire period of the study (Group F), while 26 patients never received folate (Group NF). The remaining 16 patients who did not take folate on a regular basis were excluded from subgroup analysis. Total homocysteine and creatinine plasma levels were assayed at entry into the study (time 0) and at the end of the study, 12 months later (time 12).
  
  
  RESULTS
  Homocysteinemia increased significantly from time 0 to time 12 (p < 0.001), regardless of creatinine plasma levels (p = 0.03) and folate intake (p < 0.01). However, total homocysteine levels were lower in Group F compared to Group NF at time 0 and time 12 (p < 0.02). On multivariate analysis, time of follow-up, serum creatinine and lack of folate intake were positive independent predictors of total homocysteine.
  
  
  CONCLUSIONS
  Homocysteinemia increased over time in heart transplant recipients, regardless of renal function and folate administration. Lower total homocysteine levels were associated with folate intake, suggesting that folate supplements may play a role in the prevention of vascular allograft disease.
authors.affiliation: Institute of Cardiovascular Diseases, University of Bologna, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Potena
authors.forename: F
authors.initials: F
authors.lastname: Grigioni
authors.forename: G
authors.initials: G
authors.lastname: Magnani
authors.forename: S
authors.initials: S
authors.lastname: Sorbello
authors.forename: S
authors.initials: S
authors.lastname: Sassi
authors.forename: L
authors.initials: L
authors.lastname: Marinucci
authors.forename: R
authors.initials: R
authors.lastname: Conti
authors.forename: V
authors.initials: V
authors.lastname: Carinci
authors.forename: O
authors.initials: O
authors.lastname: Leone
authors.forename: G
authors.initials: G
authors.lastname: Arpesella
authors.forename: S
authors.initials: S
authors.lastname: Coccheri
authors.forename: C
authors.initials: C
authors.lastname: Magelli
authors.forename: A
authors.initials: A
authors.lastname: Branzi
mesh_terms: D003404:Creatinine / Q000494:pharmacology*; D016572:Cyclosporine / Q000494:pharmacology*; D005260:Female; D005492:Folic Acid / Q000494:pharmacology*; D005500:Follow-Up Studies; D016027:Heart Transplantation; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D007668:Kidney / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies
chemical_list: D007166:Immunosuppressive Agents; D006710:Homocysteine; D016572:Cyclosporine; D005492:Folic Acid; D003404:Creatinine