Role of Glutathione S-Transferase Polymorphisms and Chronic Allograft Dysfunction

Autor: Eny Maria Goloni-Bertollo, Mario Abbud-Filho, Patrícia Matos Biselli, R.G. Pagliuso, M.A.S. Ferreira-Baptista, Érika Cristina Pavarino-Bertelli, M.P.S. Alvarenga, Joice Matos Biselli
Rok vydání: 2008
Předmět:
Zdroj: Transplantation Proceedings. 40:743-745
ISSN: 0041-1345
DOI: 10.1016/j.transproceed.2008.03.008
Popis: Polymorphisms within genes encoding glutathione S-transferases (GSTs) may affect responses against damage induced by oxidative stress and therefore play a role to prevent chronic allograft dysfunction (CAD). In the present study, we estimated the frequencies of GSTM1 - and GSTT1 -null genotypes among 227 renal transplant recipients seeking to establish an association with CAD. Patients persistently displaying serum creatinine (sCr) values ≤ 1.5 mg/dL, measured creatinine clearances (CLcr) ≥ 50 mL/min/1.73 m 2 , and 24-hour proteinuria ≤ 500 mg were classified as normal graft function (NF; n = 107). In contrast, the CAD group ( n = 120) presented sCr > 1.5 mg/dL, CLcr 2 , and proteinuria > 500 mg. The GSTM1 and GSTT1 polymorphisms were evaluated by the multiplex polymerase chain reaction. The frequencies of GSTT1 -null genotypes in NF and CAD cohorts were 15% and 24.2%, respectively ( P = .057), while GSTM1 -null genotypes in the same groups of patients were 44% and 46.7% ( P = .389). A combination of null genotypes for GSTT1 and GSTM1 was observed in 9.2% of patients with CAD and in 5.6% of those with NF ( P = .449). This study did not show an association of either GSTT1 - and GSTM1 -null genotypes with CAD. It is likely that development and progression of CAD are determined by a combination of complex genetic traits resulting from the interplay of several genes rather than a single gene.
Databáze: OpenAIRE