title: Insulin resistance and insulin secretion in renal transplant recipients with hepatitis C.
abstract: BACKGROUND
  Several reports have suggested an association between hepatitis C virus (HCV) infection and new-onset diabetes after transplantation (NODAT). NODAT is a common complication after renal transplantation, and it has been associated with increased long-term morbidity and mortality. HCV-positive recipients may have abnormal glucose metabolism, even though NODAT has never been previously diagnosed. The aim of this study was to analyze the pathogenic factors responsible for glucose metabolism in a series of HCV-positive renal transplant recipients.
  
  
  METHODS
  The study population comprised 16 renal transplant patients who received their grafts from deceased or living donors with anti-HCV antibodies. HCV-negative transplant recipients were individually matched with these HCV-positive recipients by year of transplantation, sex, age, serum creatinine levels, and type of calcineurin inhibitors. None of the patients had been diagnosed with diabetes. Insulin secretion and insulin resistance were determined by a 75-g oral glucose tolerance test (OGTT) and compared between the 2 groups. Categories of glucose tolerance were defined according to World Health Organization criteria.
  
  
  RESULTS
  Glucose intolerance (impaired fasting glucose, impaired glucose tolerance, diabetes mellitus) as assessed by OGTT was detected in 7 of the HCV-positive recipients (43.8%) and 3 of the HCV-negative recipients. The homeostasis model assessment of insulin resistance was greater in the HCV-positive recipients than in the HCV-negative recipients. The homeostasis model assessment of β-cell function was higher in the HCV-positive recipients than in the HCV-negative recipients.
  
  
  CONCLUSIONS
  The frequency of glucose intolerance tended to be higher in HCV-positive recipients. Furthermore, insulin resistance was greater and insulin secretion higher in HCV-positive recipients, which indicated that the increase in insulin secretion compensated for insulin resistance observed in these patients. However, HCV-positive renal transplant recipients may ultimately develop NODAT as this compensation diminishes with time.
authors.affiliation: Department of Urology, Osaka City University Graduate School of Medicine, Osaka, Japan. m9492120@msic.med.osaka-cu.ac.jp
authors.forename: J
authors.initials: J
authors.lastname: Uchida
authors.forename: T
authors.initials: T
authors.lastname: Iwai
authors.forename: Y
authors.initials: Y
authors.lastname: Machida
authors.forename: N
authors.initials: N
authors.lastname: Kuwabara
authors.forename: K
authors.initials: K
authors.lastname: Kabei
authors.forename: N
authors.initials: N
authors.lastname: Kumada
authors.forename: T
authors.initials: T
authors.lastname: Nakatani
mesh_terms: D000328:Adult; D005260:Female; D005951:Glucose Tolerance Test; D006526:Hepatitis C / Q000601:surgery*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000503:physiopathology; D016030:Kidney Transplantation; D008297:Male
chemical_list: D007328:Insulin