OBJECTIVE: To investigate the association between transforming growth factor beta-1 (TGF-beta1) gene polymorphism and chronic allograft nephropathy (CAN). METHODS: Fifty patients with failed renal allografts and clinically and histopathologically confirmed CAN were enrolled in this study along with another 50 renal transplant recipients with normal graft function. The DNA extracted from whole blood of the patients was amplified with PCR with sequence-specific primers for determining TGF-beta1 genotypes (position +869, codon 10 and position +915, codon 25). According to documented descriptions, the patients were classified into high and moderate-to-low cytokine production genotypes. The distribution frequencies of high production genotypes was then compared between CAN and non-CAN groups. To eliminate interference in the analysis of the association between TGF-beta1 polymorphism and CAN, other possible risk factors for CAN were screened, including the patients' gender, age, HLA match, delayed graft function, acute rejection, immunosuppressive regimen, cytomegalovirus infection, hypertension, and high cholesterol. RESULTS: CAN patients showed significantly greater proportion of high cytokine production genotype than the non-CAN group [70% (35/50) vs 38% (19/50), Chi(2)=10.306, P=0.001). Of the screened risk factors for CAN, only acute rejection showed some difference between the two groups, but analysis after subgrouping according to acute rejection did not suggest its influence on CAN, which supports the result that the rate of high production genotype was significantly higher in CAN group than in the non-CAN group. CONCLUSION: Most CAN patients have high TGF-beta1 production genotype, which might be a risk factor for CAN after renal transplantation. TGF-beta1 genotyping can be of value in predicting the risk of CAN after renal transplantation.
OBJECTIVE: To investigate the association between transforming growth factor beta-1 (TGF-beta1) gene polymorphism and chronic allograft nephropathy (CAN). METHODS: Fifty patients with failed renal allografts and clinically and histopathologically confirmed CAN were enrolled in this study along with another 50 renal transplant recipients with normal graft function. The DNA extracted from whole blood of the patients was amplified with PCR with sequence-specific primers for determining TGF-beta1 genotypes (position +869, codon 10 and position +915, codon 25). According to documented descriptions, the patients were classified into high and moderate-to-low cytokine production genotypes. The distribution frequencies of high production genotypes was then compared between CAN and non-CAN groups. To eliminate interference in the analysis of the association between TGF-beta1 polymorphism and CAN, other possible risk factors for CAN were screened, including the patients' gender, age, HLA match, delayed graft function, acute rejection, immunosuppressive regimen, cytomegalovirus infection, hypertension, and high cholesterol. RESULTS: CAN patients showed significantly greater proportion of high cytokine production genotype than the non-CAN group [70% (35/50) vs 38% (19/50), Chi(2)=10.306, P=0.001). Of the screened risk factors for CAN, only acute rejection showed some difference between the two groups, but analysis after subgrouping according to acute rejection did not suggest its influence on CAN, which supports the result that the rate of high production genotype was significantly higher in CAN group than in the non-CAN group. CONCLUSION: Most CAN patients have high TGF-beta1 production genotype, which might be a risk factor for CAN after renal transplantation. TGF-beta1 genotyping can be of value in predicting the risk of CAN after renal transplantation.