title: Induction therapy with basiliximab allows delayed initiation of cyclosporine and preserves renal function after cardiac transplantation.
abstract: BACKGROUND
  Cyclosporine (CsA) is frequently initiated as induction therapy in patients undergoing orthotopic heart transplantation, but our experience has identified a significant rate of post-operative renal dysfunction. We therefore devised a renal-sparing cyclosporine-free induction regimen consisting of the early administration basiliximab, an interleukin-2 receptor monoclonal antibody, followed by the late initiation of cyclosporine on post-operative Day 4.
  
  
  METHODS
  Between September 1998 and December 1999, we treated 25 patients at risk for post-operative renal dysfunction (high-risk basiliximab group) with the new induction regimen and another 33 patients not at risk (low-risk CsA group) for renal dysfunction with our standard cyclosporine protocol. We identified a historical control group (1996 through 1998) of 32 patients at risk for renal dysfunction (high-risk CsA group) who had received our standard cyclosporine protocol.
  
  
  RESULTS
  The increase in serum creatinine levels after transplantation was less in the high-risk basiliximab group (-0.1 +/- 0.7) than in the high-risk CsA group (0.5 +/- 1.0, p < 0.02) and comparable to the low-risk CsA group (0.03 +/- 0.6). The basiliximab protocol did not increase rejection; the percentage of rejection episodes was high-risk basiliximab, 0; high-risk CsA, 13; and low-risk CsA, 3 (p = .13).
  
  
  CONCLUSIONS
  Basiliximab induction therapy allows delayed initiation of cyclosporine after cardiac transplantation without an increase in rejection and reduces the risk of post-operative renal dysfunction.
authors.affiliation: Heart and Lung Transplant Program, St. Paul University Hospital, Dallas, Texas, USA. rosen029@mc.duke.edu
authors.forename: Paul B
authors.initials: PB
authors.lastname: Rosenberg
authors.forename: Ank E
authors.initials: AE
authors.lastname: Vriesendorp
authors.forename: Mark H
authors.initials: MH
authors.lastname: Drazner
authors.forename: Daniel L
authors.initials: DL
authors.lastname: Dries
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Kaiser
authors.forename: Linda S
authors.initials: LS
authors.lastname: Hynan
authors.forename: J Michael
authors.initials: JM
authors.lastname: Dimaio
authors.forename: Daniel
authors.initials: D
authors.lastname: Meyer
authors.forename: W Steves
authors.initials: WS
authors.lastname: Ring
authors.forename: Clyde W
authors.initials: CW
authors.lastname: Yancy
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D000077552:Basiliximab; D003404:Creatinine / Q000097:blood; D016572:Cyclosporine / Q000627:therapeutic use*; D005260:Female; D006084:Graft Rejection / Q000517:prevention & control; D006085:Graft Survival / Q000187:drug effects*; D016027:Heart Transplantation / Q000276:immunology* / Q000401:mortality; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D007668:Kidney / Q000187:drug effects* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D007166:Immunosuppressive Agents; D011993:Recombinant Fusion Proteins; D016572:Cyclosporine; D000077552:Basiliximab; D003404:Creatinine