Objective. The impacts of hepatitis C virus (HCV) and hepatitis B virus (HBV) infections on patient and renal graft survivals are controversial. This study sought to evaluate the effects of pretransplantation HCV and HBV infections on renal transplant patients and their grafts at our center. Patients and Methods. We retrospectively examined 1224 renal transplantations performed between 1992 and 2006, including 28 HBsAg positive; 64, anti-HCV; 9, anti-HCV plus HBsAg positive; and 1123, negative for anti-HCV and HBsAg. The mean posttransplantation follow-up was 5.6 Ϯ 4.1 years.Results. The prevalences of HBV infection were 6.2% in 1994 and 2.3% in 2006 and those of HCV infection were 6.8% in 1998 and 5.2% in 2006. The rejection rate was higher among HBVϩ (46.4%) and HCVϩ (40.6%) groups than the negative groups (31.5%), but it was not significant. There were no significant differences in patient and graft survivals among the groups. The major cause of patient death was liver failure among patients with concomitant HBVϩ and HCVϩ infections and cardiovascular disease among HCVϩ and negative patients. Conclusions. There has been a decrease in the prevalence of recipients with hepatitis virus infections over the last 15 years. Patient and graft survivals were not affected by HCV or HBV infection.
In our study, intensity of tubulointerstitial AA was shown to be a predictor of initiation of dialysis, and E-cadherin loss intensity was associated to CAI progression. However, prospective and larger studies are needed to evaluate the predictive value of these markers.
Background and Aims: Hepatitis Delta virus (HDV) genotype 3 is responsible for outbreaks of fulminant hepatitis in Northeastern South America. This study investigates if systemic inflammatory molecules are differentially expressed in patients with advanced fibrosis chronically infected with Hepatitis Delta virusgenotype 3(HDV-3). Methods: Sixty-one patients from the north of Brazil coinfected with hepatitis B virus (HBV)/HDV-3 were analyzed. HDV quantification and genotyping were performed by semi-nested real-time polymerase chain reaction (RT-PCR) and restriction fragment length polymorphism (RFLP) methodologies. Ninety-two systemic inflammatory molecules (SIMs) were measured by Proximity Extension Assay (PEA) technology. The Shapiro–Wilk, Student’s t-test, Mann–Whitney tests, and logistic regression analysis were used when appropriate. Results: The median age was 41 years, and all patients were HBeAg negative. Advanced fibrosis or cirrhosis was diagnosed by histological staging in 17 patients, while 44 presented with minimal or no fibrosis. Advanced necroinflammatory activity correlated positively with serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Established non-invasive fibrosis scores (APRI, FIB-4, and AST/ALT ratio) revealed low sensitivities and positive predictive values (PPVs) with an AUROC maximum of 0.586. Among the 92 SIMs analyzed, MCP.4, CCL19, EN.RAGE, SCF, and IL18 showed a positive correlation with fibrosis stage. A combined score including CCL19 and MCP.4 revealed a sensitivity of 81% and an odds ratio of 2.202 for advanced fibrosis. Conclusions: Standard non-invasive fibrosis scores showed poor performance in HDV-3 infection. We here suggest that the determination of CCL19 and MCP.4 may be used to identify patients with advanced fibrosis. Moreover, this study gives novel insights into the immunopathogenesis of HDV-3 infection.
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