Oxidative stress and inflammation in long-term renal transplanted hypertensives.

ABSTRACT

INTRODUCTION: Several studies have shown that chronic renal failure (CRF) is characterized by "accelerated atherosclerosis". More recent studies emphasize that inflammation and oxidative stress play a central role in atherosclerosis, and it is well-established that C-reactive protein (CRP) is a cardiovascular risk marker in the general population, in end-stage renal disease (ESRD) patients and in allograft recipients. METHODS: We measured the serum concentration of high sensitivity CRP, TNFalpha, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha, an in vivo oxidative stress marker) in 15 CRF patients and in 15 transplant recipients. Exclusion criteria were age < 30 and > 65 years, smoking, diabetes mellitus and history of cardiovascular diseases. Immunosuppressive therapy was not withdrawn, and antihypertensive treatment was the same for both groups. Systolic (SBP) and diastolic blood pressure (DBP), serum creatinine (sCr) and estimated glomerular filtration rate (GFR) were also evaluated. 15 healthy subjects were enrolled as controls. RESULTS: The transplanted group showed significantly higher values than controls of CRP (p < 0.05), TNFalpha (p < 0.05), 8-iso-PGF2alpha (p < 0.05). The CRF group as well exhibited, in comparison with controls significantly higher concentrations of CRP (p < 0.05), TNFalpha (p < 0.05), and 8-iso-PGF2alpha (p < 0.05). SBP, DBP and sCr were not different between transplanted and CRF patients. CRP was higher in transplant recipients than in CRF patients (p < 0.05). No difference in TNFalpha levels between the 2 groups was found. 8-iso-PGF2alpha was significantly higher in CRF than in the transplanted group (p < 0.05). In this latter, 8-iso-PGF2alpha showed a positive correlation with TNFalpha (p < 0.001), sCr (p < 0.001), SBP (p < 0.05) and DBP (p < 0.05). In the same group both 8-iso-PGF2alpha and TNFalpha were negatively correlated with GFR (r = -0.873 and -0.912, respectively, p < 0.001 for both). CONCLUSION: Our data have shown the coexistence of an increased oxidative stress and an inflammatory state in long-term renal graft recipients.