title: Long-term follow-up after conversion from tacrolimus to cyclosporin in renal transplant patients with new-onset diabetes mellitus after transplantation.
abstract: BACKGROUND
  The relationship between anticalcineurin (CNI) drugs and the development new-onset diabetes mellitus after kidney transplantation (NODAT) is well established. Among these agents cyclosporine shows lesser diabetogenicity than tacrolimus. It has been described that conversion from tacrolimus to cyclosporine improves glycemic control; however, there are no studies showing whether this reduced risk is maintained upon long-term follow-up.
  
  
  OBJECTIVE
  To evaluate whether CNI drugs conversion from tacrolimus to cyclosporine helps to maintain better glycemic control.
  
  
  METHODS
  We retrospectively evaluated the evolution of glucose metabolism at 5 years after conversion from tacrolimus to cyclosporine in eight patients (six men) with NODAT. Mean age was 42.8 ± 15 years, and time after transplantation to conversion 128 ± 40 months. We analyzed fasting serum glucose, lipid metabolism, renal function, and cyclosporine levels at 0, 6, 12, 24, 36, 48, and 60 months after conversion.
  
  
  RESULTS
  At 6 months after conversion, improved glucose metabolism was observed (268 ± 161 versus 121 ± 31 mg/dL; P < .01) although it was minimal in one case with persistent high blood glycemic levels. Only two patients maintained a normal glucose at the end of follow-up. Five subjects showed increased glycemia at 12 to 24 months after conversion requiring antidiabetic therapy: three patients, insulin and two oral antidiabetic agents. Two patients lost their allografts due to chronic rejection at 32 and 50 months respectively. Among the other six patients, renal function remained stable (1.9 ± 0.6 versus 2.11 ± 0.97 mg/dL; P = NS). There was no significant differences among the other variables. Cyclosporine levels remained stable during the follow-up.
  
  
  CONCLUSIONS
  Conversion of renal transplant patients with NODAT from tacrolimus to cyclosporine improves glucose metabolism in the short term but glycemia increases thereafter.
authors.affiliation: Nephrology Service and Renal Transplant Unit, Hospital Clinic, Barcelona, Spain.
authors.forename: F
authors.initials: F
authors.lastname: Batista
authors.forename: I
authors.initials: I
authors.lastname: Auyanet
authors.forename: J-V
authors.initials: JV
authors.lastname: Torregrosa
authors.forename: F
authors.initials: F
authors.lastname: Oppenheimer
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D065095:Calcineurin Inhibitors; D002908:Chronic Disease; D016572:Cyclosporine / Q000009:adverse effects* / Q000097:blood; D003920:Diabetes Mellitus / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy; D057915:Drug Substitution; D005260:Female; D006084:Graft Rejection / Q000276:immunology; D006085:Graft Survival / Q000187:drug effects; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000009:adverse effects* / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology; D016030:Kidney Transplantation / Q000009:adverse effects*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D016559:Tacrolimus / Q000009:adverse effects*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D065095:Calcineurin Inhibitors; D007004:Hypoglycemic Agents; D007166:Immunosuppressive Agents; D008055:Lipids; D016572:Cyclosporine; D016559:Tacrolimus