In Renal Transplanted Patients Inflammation and Oxidative Stress Are Interrelated

IntroductionThe 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.MethodsWe 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).ResultsBoth 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).ConclusionWe observed the coexistence of increased oxidative stress and an inflammatory state among renal graft recipients.