combined pretransplantation seropositivity of kidney transplant recipients for cytomegalovirus antigens [pp150 and pp28] a predictor for protection against infection?

This study was aimed at detecting antibodies to the antigens which may contribute to protection against cytomegalovirus [CMV] infection after organ transplantation. A total of 203 kidney transplant patients were enrolled in the study. Based on CMV antigenemia assay, 23 patients were antigen-positive and of the remaining 180 antigen-negative patients, 46 were selected as controls matched for age, gender and source of kidney. The 69 kidney recipients [KR] had CMV antibody due to previous infection and were followed up for a period of 6 months after transplantation for the development of active CMV infections by the antigenemia assay. Antibody responses to five CMV-related peptide antigens [pp65, gB, pp150, pp28 and pp38] were investigated by enzyme immunoassay and their presence was correlated with the results of the CMV antigenemia assay. Of the five CMV-related peptide antigens, only gB antigen showed response to the antibody in 10/23 [43.5%] antigen-positive patients and 9/46 antigen-negative patients and the difference was statistically significant [p = 0.048]. On the other hand, there was no significant difference in antibody responses between the antigen-positive and antigen-negative KR to the other four CMV peptide antigens [p > 0.05]. However, among the antigen-positive KR there was only 1 patient who had antibodies to both pp150 and pp28 antigen, while among the antigen-negative KR, 22 of 46 [47.8%] had the antibodies [p < 0.001]. The findings suggest that the combined presence of antibodies against the pp150 and pp28 antigens may indicate a lower risk of CMV reactivation after kidney transplantation

Modulation of the transforming Growth factor beta1 by Vitamin E in early nephropathy

The aim of this study was to investigate the pharmacological activity of an antioxidant, a-tocopherol [vitamin E, VE] in streptozotocin-induced diabetic rats and study its role in modulating the transforming growth factor 31 [TGF-beta1]. Male Sprague-Dawley rats were treated with streptozotocin to induce diabetes. VE and/or insulin [INS] were administered daily during treatment periods of 3, 5, 7 and 10 days. Plasma glucose and fructosamine were measured in diabetic rats at the end of each treatment period. Samples of plasma, urine and renal cortex were analyzed for changes in protein and lysozyme excretion, reduced glutathione and malondial-dehyde formation. TGF-beta1 was determined by ELISA and expression of TGF-beta1 mRNA was investigated by RT-PCR and Northern blot analysis. Diabetes-induced glycemic stress was suppressed by INS, VE or a combination of INS and VE. Diabetes-induced increases of glucose, protein and lysozyme excretion were markedly depressed after 10-day treatment with INS, VE and the combination of INS and VE. Decreased glutathionecontent in the renal cortex of diabetic rats recovered towards control values, especially after 10-day treatment. Malondialdehyde content increased in diabetic rats and was reduced towards control value following 7- and 10-day treatments. Treatment of diabetic rats with INS, VE or the combination of INS and VE decreased elevated TGF-beta1 in plasma, decreased excretion of TGF-beta1 in urine, and decreased renal cortex TGF-beta1 mRNA levels. Conclusions: Diabetes-induced overexpression of TGF-beta1 mRNA was suppressed by VE and INS after 5-, 7- and 10-day treatments. The results obtained with the antioxidant VE suggest that oxidative stress is involved in the development of diabetic nephropathy. Therefore, VE treatment may be effective in early stages of diabetic nephropathy to decrease or prevent pathological complications