https://www.ajkd.org/article/S0272-6386(03)00828-X/pdf

Hepatitis C and renal disease: an update

MODES OF TRANSMISSION TOBIAS HEINTGES AND JACK R. WANDS HCV is generally transmitted by the parenteral route. Well known and common modes of transmission involve transfuHepatitis C virus (HCV) is an RNA virus with a genomic size of 9.6 kb. More than 50% of individuals exposed to HCV sions and/or parenteral contact with blood products. However, up to 50% of individuals deny exposure to any of these develop chronic infection. Of those individuals chronically infected, approximately 20% to 30% will develop liver cirrhoknown risk factors, and infection is often designated as ‘‘community acquired.’’ Before the initiation of HCV antibody sis and/or hepatocellular carcinoma when followed for twenty to thirty years. Methods to identify HCV include a screening, approximately 10% to 20% of individuals, who had received multiple blood transfusions or plasma products, highly sensitive third generation immunoassay that detects antibodies to structural and nonstructural proteins in serum. seroconverted to anti-HCV positive. Thus, the relative risk was 0.45% per unit transfused. However, the introduction Viremia may be detected by reverse transcriptase–polymerase chain reaction (RT–PCR) technology. The role of HCV of routine HCV antibody screening of blood products has led to a sharp decrease in the transmission rate of HCV. For infection in acute and chronic liver disease has recently be

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.510260338

Hepatitis C virus: Epidemiology and transmission

https://www.ajkd.org/article/S0272-6386(01)02061-3/pdf

Hepatitis C virus infection and renal transplantation

Background. Chronic liver disease is one of the most important complications after renal transplantation. Hepatitis B and mainly hepatitis C are the more frequent causes of liver disease. Although there are controversial results, in some series, hepatitis B and hepatitis C are associated with lower graft and patient survival. Patients and methods. A total of 3365 adult patients who received a renal transplant in 1990 (N ¼ 824), 1994 (N ¼ 1075) and 1998 (N ¼ 1466) with a functioning graft after the first year were included. Fifty-one (2.1%) with positive HbsAg were diagnosed with hepatitis B at transplantation; 488 (16.9%) presented positive anti-hepatitis C antibodies and were diagnosed with hepatitis C virus (HCV) infection and 25 patients (0.8%) were diagnosed with concomitant hepatitis B virus (HBV) and HVC infection. Demographic, immunosuppression, survival figures and post-transplant and follow-up data of these patients and negative HBV and HVC patients were recorded. Results. The overall prevalence of HBV in the recipients was 2.1%. Patient survival was lower and liver disease was the main cause of death in HBVpositive patients. However, in the multivariate analysis the presence of positive HbsAg did not have an independent risk factor for graft loss and patient death. This finding was similar in patients with concomitant HBV and HVC infection. Graft and patient survival were lower in HCV-positive patients and liver disease was the main cause of death. Interestingly, proteinuria and serum creatinine were risk factors for graft loss and patient death. Fortunately, prevalence of HCV in the recipients significantly decreased from 29% in 1990 to 10% in 1998. Conclusions. In the last decade in Spain, HBV infection in the recipients, showing an overall prevalence � 2%, did not influence graft and patient survival. However, HCV infection in the recipient was associated with lower graft and patient survival, although the prevalence of HCV clearly decreased from 29% in 1990 to 10% in 1998.

The influence of hepatitis B and hepatitis C virus infection in the recipient on late renal allograft failure

https://www.ajkd.org/article/S0272-6386(03)01225-3/pdf

The impact of hepatitis C virus viremia on renal graft and patient survival: a 9-year prospective study.

The aim of the study was to analyse the influence of co-infection by hepatitis B virus (HBV) and hepatitis C virus (HCV) as compared with HCV infection alone in 1098 patients who received a kidney transplant between 1 January and 31 December 1991. At transplantation, the prevalence of anti-HCV antibodies was 21.40% (235/1098) while the prevalence of HBV infection was 9.85% (108/1096); 46 patients were co-infected with HBV and HCV, either 19.70% of HCV-infected patients and 42.60% of HBV-infected patients. Liver tests, galactose clearance and liver biopsy were compared in the 46 co-infected patients (HCV+HBV+) and in the 189 HCV-infected patients (HCV+HBV-). At the time of transplantation, cytolysis was present in 31.45% of HCV+HBV- patients (50/159) and in 40% of HCV+HBV- patients (16/40); cholestasis was present in 34.18% of HCV+HBV- patients (34/158) and 42.11% of HCV+HBV+ patients (16/38). At 6 months the incidence of biological abnormalities increased to 37% in HCV+HBV- patients (55/150) and to 52.5% in HCV+HBV+ patients (21/40), suggesting a more deleterious effect of the immunosuppressive therapy in the co-infected group. Over the course of transplantation, chronic hepatitis was present in 50% of HCV+HBV- patients and in 64.1% of HCV+HBV+ patients. Liver failure occurred in 7% of HCV+HBV- patients (12/156) and 17% of HCV+HBV+ patients (7/41). Galactose clearance was performed as a functional test in 68 patients: it was not significantly different in either group. Liver biopsy was performed in 108 patients at least once.(ABSTRACT TRUNCATED AT 250 WORDS)

Co-infection by hepatitis B virus and hepatitis C virus in renal transplantation: morbidity and mortality in 1098 patients

In organ transplantation, virus transmitted by the donor is associated with a higher risk of severe primary infection after transplantation in the seronegative recipient. In this study, the risk of hepatitis-C virus (HCV) transmission by the kidney was determined, and the morbidity in the recipient assessed. Serum samples from all kidney donors of our Transplantation Unit between 1983 and 1988 were screened for antibodies to anti-HCV by first enzyme-linked immunosorbent assay (Ortho ELISA) and positive samples were confirmed by a second-generation ELISA and the CHIRON RIBA HCV test. Of the 164 kidney donors whose sera were available, five were positive (3%) and all of them were positive with the RIBA test. Liver function was normal in the five donors. Seven recipients received a renal transplant from the anti-HCV-positive donors. Two patients had a follow-up too short to draw any conclusions. Two patients remained anti-HCV-negative up to 36 and 48 months, respectively, but one of them had chronic hepatitis. One patient was anti-HCV-positive before transplantation and remained positive over the 4-year follow-up. The two last patients seroconverted and acute hepatitis occurred at 16 and 101 days after transplantation, respectively. In both cases, no peroperative or postoperative transfusion was given and no other cause of hepatitis could be determined. A cirrhotic evolution was observed within 15 and 36 months in both cases. Thus HCV can be transmitted by a kidney transplant and cadaveric donors positive for anti-HCV antibodies should be excluded from kidney donation.

Should hepatitits-C virus antibody-positive donors be excluded from kidney donation?

The aim of the study was to evaluate the virological parameters associated with the severity of cytomegalovirus (CMV) disease in renal and simultaneous renal and pancreatic transplantation. The association of the viral profile and the severity of the viral disease was analysed taking into account different confounding variables susceptible to linkage with the severity of the CMV infection and the viral parameters. All the patients transplanted between 1 January 1989 and 31 December 1990, a total of 242, were prospectively followed by viral cultures in blood and urine and by serological methods using the detection of CMV-specific IgM and the complement fixation (CF) test. The samples were taken systematically each week for the first month and then at day 90, 180 and every 6 months and also in cases of clinical manifestations related to viral disease. CMV infection was diagnosed virologically by the presence of viraemia, viruria, IgM, or a significant rise in CMV antibody titre in CF. CMV disease was classified as asymptomatic, mild (fever and/or leukopenia), moderate (fever, leukopenia and liver abnormalities), severe (CMV pneumopathy and/or gastrointestinal disease) or fatal. The incidence of CMV infection was 65% (157/242): 32% asymptomatic, 36% mild, 30% moderate and 2% severe. The presence of IgM was associated with the severity of CMV disease: 51.4% of moderate and severe CMV infections in the group with IgM versus only 16% in the group without IgM (P < 0.0001). The risk of having severe or moderate CMV disease was 3.28 times higher in patients with positive IgM. However the serological changes in CF were not significantly associated with the severity of the viral disease since 34.6% of the patients with CF changes had a severe form versus 20.8% in the group without CF modification. Viruria was significantly associated with moderate or severe infection: 43.6% of the patients with viruria had severe infection versus only 12.5% in the patients without viruria (P < 0.0002). The risk of having moderate or severe CMV disease was 3.48 times higher in the patients with viruria. Viraemia was also associated with more severe CMV infection: 48.6% of moderate or severe CMV infection in the group of patients with viraemia versus 19% in the group without viraemia (P < 0.0001). The risk of having severe or moderate CMV infection was 2.58 times higher in the patients with viraemia. Viraemia was not more associated with severe CMV infection than viruria. Using the maximum likelihood ratio method and the logistic regression model, CMV-specific IgM, viruria and viraemia were each shown to be associated with the severity of CMV disease and the addition of one parameter to the other(s), whatever the type (except the CF changes) and whatever the order of this addition, did not remove the link between the severity and IgM, viruria and viremia. The incidence of severe and moderate CMV disease increased with the number of positive viral parameters (PVP) from 2% of moderate and severe infections in the group with one PVP, to 28% in the group with two PVP, to 39% in the group with three PVP and 68% in the group with four PVP (trend, 35.95; P < 0.0001). Taking the absolute risk of the group of patients without IgM, viruria or viraemia as the basal level, the observed relative risk of severe CMV infection varied from 6.45 in the group with positive IgM without viruria or viraemia, to 10.74 in the group with positive IgM and viruria without viraemia and to 22.5 in the group with the three positive parameters IgM, viruria and viraemia. The different potential confounding factors (recipient and donor serology, renal or renal and pancreatic transplantation, DR compatibility, rejection before CMV infection) did not modify the link between the viral profile and the severity of CMV disease. This study suggests that the severity of CMV disease might be linked to the overspread of the virus as well as to the consequences of a CMV-specific humoral immune response.

Cytomegalovirus (CMV) excretion as a factor in the severity of CMV disease in kidney and simultaneous kidney and pancreas transplantation.

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Co-infection by hepatitis B virus and hepatitis C virus in renal transplantation: morbidity and mortality in 1098 patients

Should hepatitits-C virus antibody-positive donors be excluded from kidney donation?

Cytomegalovirus (CMV) excretion as a factor in the severity of CMV disease in kidney and simultaneous kidney and pancreas transplantation.