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Glutathione S-transferase T1 deletion is a risk factor for developing end-stage renal disease in diabetic patients
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2004
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Metabolic DisorderGeneticsGenetic EpidemiologyDiabetic PatientsFree Radical MetabolismInsulin SignalingOxidative StressMetabolic SyndromeRenal FunctionRisk FactorChronic Kidney DiseaseHealth SciencesBiochemistryKidney FailureEnd-stage Renal DiseaseUrologyRenal DiseaseGenetic DeterminantDiabetesPhysiologyDiabetic Kidney DiseaseReactive Oxygen MetabolitesDiabetes MellitusMedicineNephrologyKidney Research
Reactive oxygen metabolites may contribute to the development of end-stage renal disease (ESRD) in diabetic and hypertensive patients. In this study, we used multiplex polymerase chain reaction (PCR) to analyze polymorphisms of two endogenous antioxidant genes, glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1), and to determine their role in the development of ESRD in diabetic and hypertensive patients. Our results showed that homozygous deletion of the GSTT1 gene is a risk factor for developing ESRD in diabetic patients (p=0.004, OR=2.18, 95% confidence interval (CI) =1.29-3.70), but not in hypertensive patients. No association between homozygous deletion of GSTM1 and the development of ESRD was found in either diabetic patients or hypertensive patients. These results indicate that genetic variations in enzymes involved in free radical metabolism are associated with the development of ESRD in diabetes mellitus (DM) patients, and may permit the targeting of preventive and early intervention strategies to high-risk individuals.