In renal transplanted patients inflammation and oxidative stress are interrelated.

Introduction: The inflammatory state plays a well-documented role to cause oxidative stress, especially in end-stage renal disease (ESRD) patients, wherein several cardiovascular risk factors are amplified by the coexistence of a microinflammatory state with increased oxidative stress. Methods: We measured serum concentrations of high sensitivity C-reactive protein (CRP), tumor necrosis factor α (TNFα), 8-iso-prostaglandin F2α (8-iso-PGF2α-in vivo oxidative stress marker) in 15 chronic renal failure (CRF) and 15 transplant patients versus 15 healthy controls. Exclusion criteria were: age <30 or >65 years as well as a diagnosis of diabetes or cardiovascular diseases. We evaluated systolic (SBP) and diastolic blood pressure (DBP), serum creatinine (sCr), and glomerular filtration rate (GFR). Results: Both the transplanted and the CRF group showed significantly higher values of CRP, TNFα, and 8-iso-PGF2α than the controls (P < .05 for all). SBP, DBP, and sCr were not different between transplanted and CRF patients. CRP was higher in transplant recipients than in CRF patients (P < .05). No difference in TNFα levels was observed between the two groups. 8-iso-PGF2α was significantly higher in the CRF than in the transplanted group (P < .05), although the latter cohort showed a positive correlation between 8-iso-PGF2α and TNFα (P < .001), sCr (P < .001), SBP (P < .05), and DBP (P < .05). In the same group both 8-iso-PGF2α and TNFα were negatively correlated with GFR (r -.824 and -.866, respectively; P < .001 for both). Conclusion: We observed the coexistence of increased oxidative stress and an inflammatory state among renal graft recipients.