title: Gene polymorphisms are associated with posttransplantation diabetes mellitus among Taiwanese renal transplant recipients.
abstract: BACKGROUND
  Genetic variations may affect posttransplantation metabolic syndrome and diabetes mellitus (PTDM), which is associated with greater morbidity and progressive impairment of both patient and graft survivals. The aim of this study was to evaluate several candidate gene polymorphisms for their association with the risk of developing PTDM.
  
  
  METHODS
  In April 1999, we enrolled 278 renal transplant participants, including 251 subjects free of diabetes and 27 with PTDM. We studied several candidate gene polymorphisms associated with diabetes: 4G/5G polymorphism of plasminogen activator inhibitor 1 (PAI-1) at -675; C/T polymorphism of interleukin-1beta (IL-1β) at -511; G/C polymorphism of IL-6 at 174; polymorphic XbaI of Glucose transporter 1 (GLUT1); and C/T polymorphism of methylenetetrahydrofolate redutase (MTHFR) at 677.
  
  
  RESULTS
  The PTDM group had an older mean age (47.6 ± 9.8 years), greater predominance of men (77.8%), higher number of chronic diseases (CDN ≥2, 96.3%), and more patients using tacrolimus-based immunosuppression (44.4%; P < .05). Using model A, a simple logistic regression, we observed that patients with the IL-6 G/G genotype experienced a lower risk of developing PTDM (odds ratio [OR], 0.08; 95% confidence interval [CI] 0.01-0.86), and multiple logistic regression models B and C, after adjusting for different variables, confirmed this observation (model B: OR, 0.05; 95% CI, 0.00-0.66). The IL-6 G/G genotype showed a borderline effect in model C (OR, 0.02; 95% CI, 0.00-1.16). There were no significant differences between the 2 groups in genotype variations of PAI-1, IL-1β, GLUT-1, and MTHFR.
  
  
  CONCLUSIONS
  The G/G genotype of IL-6 may play an important role to lower the risk for PTDM development.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
authors.forename: S-C
authors.initials: SC
authors.lastname: Weng
authors.forename: K-H
authors.initials: KH
authors.lastname: Shu
authors.forename: D-C
authors.initials: DC
authors.lastname: Tarng
authors.forename: M-J
authors.initials: MJ
authors.lastname: Wu
authors.forename: C-H
authors.initials: CH
authors.lastname: Chen
authors.forename: T-M
authors.initials: TM
authors.lastname: Yu
authors.forename: Y-W
authors.initials: YW
authors.lastname: Chuang
authors.forename: S-T
authors.initials: ST
authors.lastname: Huang
authors.forename: C-H
authors.initials: CH
authors.lastname: Cheng
mesh_terms: D000328:Adult; D001483:Base Sequence; D003430:Cross-Sectional Studies; D017931:DNA Primers; D003920:Diabetes Mellitus / Q000209:etiology / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics; D011110:Polymorphism, Genetic; D013624:Taiwan
chemical_list: D017931:DNA Primers; D053583:Interleukin-1beta; D017395:Plasminogen Activator Inhibitor 1; D042965:Methylenetetrahydrofolate Reductase (NADPH2)