Treatment with N-acetylcysteine in stable renal transplantation.

The primary cause of morbidity and mortality in renal transplantation is cardiovascular disease. Increased oxidative stress implies a greater degree of atherogenesis in these patients. N-acetylcysteine (NAC) which has a thiol group that is the source of l-cysteine and reduced glutathione, acts against atherosclerosis via a decrease in apoptosis, vasoconstriction, and endothelial dysfunction. Experimental models have examined the antioxidant effects of NAC during and after ischemia-reperfusion, but few studies have shown an effect in renal transplantation in human beings. In 8 months, we studied the effect of NAC treatment on oxidative stress, lipids, and renal function in 25 patients with stable renal function and no diabetes after transplantation. Data were collected on oxidative parameters: malondialdehyde, glutathione peroxidase, catalase, superoxide dismutase, glutathione reductase, lipid profile, and renal function (creatinine concentration, Cockroft-Gault formula, and Modified Diet in Renal Disease study). There were no significant differences in oxidative profile before and after treatment with NAC. The mean serum high-density lipoprotein cholesterol fraction increased after treatment and showed a significant positive correlation with glutathione peroxidase (r = 0.495). Serum creatinine concentration decreased, and Cockroft-Gault and Modified Diet in Renal Disease study estimates of renal function increased in the treatment period. In conclusion, NAC treatment in patients with stable renal function after transplantation increased high-density lipoprotein cholesterol and antioxidant molecules in relation to glutathione peroxidase, with a positive influence on renal function.

Left ventricular structure and function in long-term kidney transplantation: the influence of glucose metabolism and oxidative stress.

Impaired cardiac structure and function are fundamental components of cardiovascular disease, leading to morbidity, mortality, and graft loss after renal transplantation. The aim of this study was to describe and determine the factors involved in these cardiac abnormalities, paying special attention to the role of glucose metabolism and oxidative stress. We studied 54 long-term, nondiabetic recipients with no valvulopathy who underwent an echocardiographic examination and simultaneous biochemical determinations of lipid profile, hemoglobin A1c (HbA1c), and various oxidative stress parameters: malondialdehyde, superoxide dismutase, total glutathione, and isoprostanes. We calculated the left ventricular mass index (LVMI) and ejection fraction and the peak velocity of early rapid filling to peak velocity of atrial filling (E/A) ratio. Left ventricular hypertrophy (LVH), systolic dysfunction, and diastolic dysfunction (LVDD) were present in 25.9%, 5.6%, and 59.25% of the patients, respectively. The mean blood pressure (MBP) was higher and the hemoglobin lower among patients with LVH, which was related to the age of the patients. We observed a significant negative association of the E/A ratio-used as an index of LVDD-with HbA1c (r = -.448, P = .002) and age (r = -.57, P = .000) and a positive association with the level of total glutathione (r = .322, P = .029). Multiple regression analysis of the E/A ratio showed significance only for HbA1c but not for MBP or LVMI. These results suggested a possible causal influence of subclinical glucose metabolism impairment as detected by HbA1c on the presentation of LVDD via the impaired oxidative stress status, independent of blood pressure control or LVH grade.