title: Prediabetic States, subclinical atheromatosis, and oxidative stress in renal transplant patients.
abstract: Prediabetic states are common among renal transplant patients, portending increased cardiovascular risk with associated carotid atheromatosis. Oxidative stress (OS) induces lipid peroxidation, a key factor in the development of atheromatosis. The aim of this study was to investigate the influence of OS and impaired glucose homeostasis status on carotid atheromatosis in nondiabetic recipients. Thirty-seven nondiabetic renal transplant patients were studied at baseline (<3 months) and at 1 and 2 years posttransplantation by ultrasound measurement of carotid intima-media thickness (CIMT), standard oral glucose tolerance test, and determination of blood markers of lipid peroxidation (8-isoprostanes [8-ISOP] and malondialdehyde [MDA]). Prediabetic state (impaired fasting glucose, impaired glucose tolerance, and provisional diagnosis of diabetes [provDM] and new-onset diabetes after transplantation [NODAT]) was classified following American Diabetes Association (ADA) criteria. Total CIMT index (TCIMT) was calculated as the sum of right and left CIMT and DeltaTCIMT as the difference in TCIMT values at 2 years (end of study) minus baseline. At baseline and 1 year, TCIMT was significantly related to 8-ISOP (r = .611; P = .002) and to recipient age (r = .654; P = .000). At 2 years, DeltaTCIMT was significantly correlated with MDA (r = .635; P = .001) with significant differences in TCIMT observed between prediabetic states and diabetes (P = .001). Multiple regression analysis identified 8-ISOP and age as factors independently associated with TCIMT and MDA with DeltaTCIMT. These results suggested that lipid peroxidation in renal transplant recipients contributed to increases in CIMT, which was more pronounced among older and diabetic (provDM or NODAT) patients.
authors.affiliation: Department of Nephrology, Hospital Universitario Virgen de las Nieves, Granada, Spain. josem.osorio.sspa@juntadeandalucia.es
authors.forename: J M
authors.initials: JM
authors.lastname: Osorio
authors.forename: C
authors.initials: C
authors.lastname: Ferreyra
authors.forename: A
authors.initials: A
authors.lastname: Pérez
authors.forename: J M
authors.initials: JM
authors.lastname: Moreno
authors.forename: A
authors.initials: A
authors.lastname: Osuna
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000961:Antilymphocyte Serum / Q000627:therapeutic use; D050197:Atherosclerosis / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000453:epidemiology; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D000077561:Daclizumab; D003920:Diabetes Mellitus / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000009:adverse effects / Q000276:immunology / Q000473:pathology* / Q000502:physiology; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011183:Postoperative Complications / Q000453:epidemiology; D011236:Prediabetic State / Q000473:pathology*; D006435:Renal Dialysis; D013997:Time Factors; D014463:Ultrasonography
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000961:Antilymphocyte Serum; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D000077561:Daclizumab