title: Angiotensinogen, angiotensine converting enzyme and plasminogen activator inhibitor-1 gene polymorphism in chronic allograft dysfunction.
abstract: Despite dramatic improvements in first-year patient and graft survival rates, chronic allograft dysfunction (CAD) remains the leading cause of late renal allograft loss, while current immunologic strategies have little effect on this condition. The renin-angiotensin system (RAS) plays an important role in progression of chronic renal disease. It was shown that plasminogen activator inhibitor-1 (PAI-1) functions in the RAS. This study investigates the possible links between angiotensinogen (AGT M235T), angiotensin-converting enzyme (ACE) and PAI-1 genotypes with CAD. Assessments of polymorphism were performed in 127 renal allograft recipients (77 with CAD and 50 with normal renal function). Fifty healthy subjects were also considered for comparison. Genotypes were determined using polymerase chain reaction (PCR) sequence-specific primers and PCR followed by restriction fragment length polymorphism analysis. Kidney recipients with CAD had significantly higher frequencies of the TT than the recipients without CAD (P < 0.05). The transplant recipients with CAD also had significantly higher frequencies of the DD genotype than those without CAD (P < 0.05). No significant differences were observed between the allelic and genotypic distributions of PAI-1 polymorphisms. Therefore, determination of AGT M235T and ACE genotypes prior to transplantation may be useful to identify patients who are at risk for chronic renal transplant dysfunction.
authors.affiliation: Organ Transplant Research Center, Nemazi Hospital, Shiraz University of Medical Sciences, Zand street, Shiraz, Iran. negarazarpira@yahoo.com
authors.forename: Negar
authors.initials: N
authors.lastname: Azarpira
authors.forename: M
authors.initials: M
authors.lastname: Bagheri
authors.forename: Gh A
authors.initials: GA
authors.lastname: Raisjalali
authors.forename: M H
authors.initials: MH
authors.lastname: Aghdaie
authors.forename: S
authors.initials: S
authors.lastname: Behzadi
authors.forename: H
authors.initials: H
authors.lastname: Salahi
authors.forename: M
authors.initials: M
authors.lastname: Rahsaz
authors.forename: M
authors.initials: M
authors.lastname: Darai
authors.forename: M J
authors.initials: MJ
authors.lastname: Ashraf
authors.forename: B
authors.initials: B
authors.lastname: Geramizadeh
mesh_terms: D000328:Adult; D000483:Alleles; D000808:Angiotensinogen / Q000235:genetics*; D002908:Chronic Disease; D003710:Demography; D005260:Female; D005838:Genotype; D006084:Graft Rejection / Q000235:genetics*; D006801:Humans; D015810:Linkage Disequilibrium / Q000235:genetics; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D012307:Risk Factors; D014019:Tissue Donors; D014184:Transplantation, Homologous
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A