title: No increase in rejection or graft loss in kidney transplant recipients with thrombophilia treated with anticoagulation and triple immunosuppression.
abstract: BACKGROUND
  Recent studies from Europe have demonstrated that patients with end-stage renal disease who receive a kidney transplant are at an increased risk for rejection and graft loss when compared with patients who have no known thrombophilia. The role of anticoagulation has not been investigated in these patients.
  
  
  METHODS
  We prospectively tested patients who were evaluated for a kidney transplant for 8 thrombophilias, protein S and C deficiencies, factor V Leiden mutation, antithrombin III deficiency, anticardiolipin antibody, lupus anticoagulant, prothrombin gene mutation, and heparin-induced platelet antibody (HIPA). Patients with any identified thrombophilia received heparin or argatroban (for HIPA (+) patients) followed by coumadin for 1 year after transplantation. Triple therapy included cyclosporine, prednisone, and CellCept (Roche Pharmaceuticals, Nutley, NJ, USA). Sensitized, black, or repeat transplantation patients received induction with an interleukin (IL)-2 inhibitor. Data were collected in a retrospective manner. Rejection was biopsy-proven.
  
  
  RESULTS
  Of the 112 transplant recipients who were tested for thrombophilia, 37 had 1 or more thrombophilia and 75 had no thrombophilia identified. Twenty-six patients received heparin and 11 received argatroban. There were no differences in recipient age, cold storage time, graft loss, HLA match, rejection episodes, 1-year graft survival, or serum creatinine level at 1 year. Significant differences were noted in posttransplantation bleeding, 35% versus 5%, and delayed graft function, 32% versus 15%, in patients with thrombophilia versus no thrombophilia, respectively.
  
  
  CONCLUSIONS
  This is the first study to demonstrate that there is no increase in rejection or graft loss in kidney transplant recipients with thrombophilia when treated with anticoagulation and triple immunosuppression.
authors.affiliation: Department of Surgery, Penn State/Hershey Medical Center, Hershey, Pennsylvania 17033, USA.
authors.forename: C R
authors.initials: CR
authors.lastname: Pagano
authors.forename: L
authors.initials: L
authors.lastname: Dawson
authors.forename: A
authors.initials: A
authors.lastname: Dick
authors.forename: S M
authors.initials: SM
authors.lastname: Lerner
authors.forename: T
authors.initials: T
authors.lastname: Valenia
authors.forename: J
authors.initials: J
authors.lastname: Braun
authors.forename: M A
authors.initials: MA
authors.lastname: Smith
authors.forename: C
authors.initials: C
authors.lastname: Farrell
authors.forename: E J
authors.initials: EJ
authors.lastname: Alfrey
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use*; D001120:Arginine / Q000031:analogs & derivatives; D003404:Creatinine / Q000097:blood; D004359:Drug Therapy, Combination; D005165:Factor V / Q000235:genetics; D005260:Female; D006084:Graft Rejection / Q000453:epidemiology*; D006085:Graft Survival / Q000502:physiology*; D006493:Heparin / Q000627:therapeutic use; D006650:Histocompatibility Testing; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016030:Kidney Transplantation / Q000276:immunology / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009154:Mutation; D010875:Pipecolic Acids / Q000627:therapeutic use; D013449:Sulfonamides; D019851:Thrombophilia / Q000150:complications / Q000188:drug therapy*; D013927:Thrombosis / Q000150:complications / Q000188:drug therapy*
chemical_list: D000925:Anticoagulants; D007166:Immunosuppressive Agents; D010875:Pipecolic Acids; D013449:Sulfonamides; C095381:factor V Leiden; D005165:Factor V; D006493:Heparin; D001120:Arginine; D003404:Creatinine; C031942:argatroban