title: No association between renin-angiotensin system gene polymorphisms and early and long-term allograft dysfunction in kidney transplant recipients.
abstract: BACKGROUND
  Genes determining the activity of the renin-angiotensin system (RAS) may be alloantigen-independent factors influencing kidney allograft function. We determined if gene polymorphisms of the RAS are associated with early and long-term post-transplantation graft dysfunction in 405 Caucasian kidney recipients with graft survivals of >2 years.
  
  
  METHODS
  We calculated the slopes of serum creatinine(-1)/year and urinary protein excretion/year to follow graft function over time. Subjects were genotyped for the deletion (D) polymorphism of the gene encoding angiotensin I-converting enzyme, the angiotensin II-receptor type1 gene 1166A-C polymorphism and the M235T polymorphism of the angiotensinogen gene.
  
  
  RESULTS
  The frequencies of factors predicting graft function were similar in patients with different genotypes. None of the polymorphisms influenced need for dialysis in the first week after transplantation, occurrence of at least one rejection episode, the slope of serum creatinine(-1)/year or the slope of urinary protein excretion/year. Results were independent of blood pressure or the use of angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers or calcineurin inhibitors. The combination of genotypes did not influence the indicators of early and long-term graft dysfunction.
  
  
  CONCLUSIONS
  Neither the investigated gene polymorphisms of the RAS in kidney allograft recipients nor their combinations have an impact on early and long-term graft dysfunction.
authors.affiliation: Center for Cardiovascular Research, Klinik für Nephrologie, Charité, Humboldt Universität, Berlin, Germany.
authors.forename: Torsten
authors.initials: T
authors.lastname: Slowinski
authors.forename: Petra
authors.initials: P
authors.lastname: Diehr
authors.forename: Patrick
authors.initials: P
authors.lastname: Kleemann
authors.forename: Lutz
authors.initials: L
authors.lastname: Fritsche
authors.forename: Lutz
authors.initials: L
authors.lastname: Renders
authors.forename: Klemens
authors.initials: K
authors.lastname: Budde
authors.forename: Ingeborg A
authors.initials: IA
authors.lastname: Hauser
authors.forename: Hans H
authors.initials: HH
authors.lastname: Neumayer
authors.forename: Berthold
authors.initials: B
authors.lastname: Hocher
mesh_terms: D000328:Adult; D000808:Angiotensinogen / Q000235:genetics; D015415:Biomarkers; D002872:Chromosome Deletion; D005260:Female; D005838:Genotype; D006084:Graft Rejection / Q000235:genetics; D006085:Graft Survival / Q000235:genetics*; D006801:Humans; D016030:Kidney Transplantation; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics*; D012307:Risk Factors; D013997:Time Factors; D014184:Transplantation, Homologous
chemical_list: D015415:Biomarkers; D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A