乙、丙型肝炎病毒感染对肾移植患者长期存活的影响

目的　了解乙型肝炎病毒（ＨＢＶ） 及丙型肝炎病毒（ＨＣＶ） 感染对肾移植患者长期存活的影响。方法　对８０ 例感染ＨＢＶ、ＨＣＶ 者肾移植术后肝病及排斥的发生情况、死亡原因及长期存活率进行分析。结果　移植后慢性肝病发生率为２１ ．２５％ , 死亡率为１８ ．７５ ％ , 显著高于非感染组（１ ．１９ ％ , Ｐ＜ ０．０１） ;ＨＣＶ 组超急性排斥及加速性排斥的发生率（６ ．０６％ ,９ ．０９ ％ ） 显著高于非感染组（０ ．７２ ％ ,２ ．７４ ％ ; Ｐ＜ ０ ．０１ , Ｐ＜ ０ ．０５）。结论　ＨＢＶ及ＨＣＶ感染显著影响肾移植受者的长期存活率; 移植后肝病及感染是其主要死因; 对ＨＢＶ 及ＨＣＶ 感染患者应采取合理的免疫抑制治疗。     

乙型肝炎病毒和丙型肝炎病毒感染对肾移植受者存活的影响

目的探讨乙型肝炎病毒(HBV)和(或)丙型肝炎病毒(hepatitis C virus,HCV)感染对肾移植受者长期存活的影响及预防措施。方法 HBV和(或)HCV感染肾移植受者110例(感染组),其中HBV感染受者56例、HCV感染受者52例,HBV与HCV合并感染2例。非HBV与非HCV感染受者694例(非感染组)。感染组受者术前有病毒复制者予积极治疗,研究早期肝功能正常者可接受肾移植,后期均用聚合酶链反应(PCR)检测,要求连续3～6个月HBV脱氧核糖核酸(DNA)0copy/ml,HCV核糖核酸(RNA)0copy/ml方可接受肾移植。术后定期检测HBV与HCV,定期检测感染组受者HBVDNA滴度、HCVRNA滴度。发现HBV复制,选用拉米夫定、阿德福韦酯治疗,酌情减少免疫抑制剂用量。分别比较两组术后1、3、5年人、肾存活率,比较两组的肝功能衰竭病死率。结果非感染组人、肾存活率分别为:1年94.2%、91.4%,3年为86.4%、85.2%,5年为82.7%、78.9%;感染组人、肾存活率分别为:1年90.2%、88.1%,3年为88.9%、86.2%,5年为81.5%、76.3%;两组数据比较差异均无统计学意义(均为P>0.05)。感染组中14例(12.7%)死于肝功能衰竭,其中10例为HBV感染者,非感染组受者无1例死于肝衰竭。感染组术后肝衰竭病死率明显高于非感染组(12.7%、0,P<0.05)。结论受者术前HBV和(或)HCV感染会明显增加肾移植术后肝衰竭死亡危险。患者术前处于病毒复制期应予积极治疗,在肝炎病毒停止复制6个月后再考虑肾移植。长期随访中应定期复查HBV与HCV感染指标,早确诊、早治疗,并及时调整免疫抑制剂剂量。     

Renal transplantation offers a better survival in HCV-infected ESRD patients

Sezer S, Ozdemir FN, Akcay A, Arat Z, Boyacioglu S, Haberal M. Renal transplantation offers a better survival in HCV-infected ESRD patients. Clin Transplant 2004 DOI: 10.1111/j.1399-0012.2004.00252.x Copyright Blackwell Munksgaard, 2004Abstract: The presence of hepatitis C virus (HCV) infection has been found to adversely affect the morbidity and mortality rates in the dialysis population. Renal transplantation is a treatment option after a careful pre-transplant evaluation. We designed this study to find the impact of HCV infection on patient survival, co-morbidity and allograft survival in a selected group of hemodialysis (HD) and transplant population. We retrospectively analyzed 116 renal transplant patients (94 HCV-negative, 22 HCV-positive) and 136 HD patients (106 HCV-negative, 30 HCV-positive) who had renal transplantation or underwent dialysis before 1996. The HCV-infected patients were evaluated by liver biopsy for the absence of advanced liver disease before transplantation. There was no clinical or laboratory decompensation of liver disease in transplant and dialysis patient groups. The overall 5-yr survival rates were 85.2% for renal transplant recipients and 74.5% for those on HD. The comparison results revealed a significant difference between HCV-infected patients with and without transplantation. The 3-yr renal allograft survival rates were comparable in HCV-positive and -negative patients, but the risk of chronic allograft nephropathy (CAN) and graft failure were higher at the fifth year in HCV-positive patients. In conclusion, renal transplantation should the preferred therapy in HCV-infected dialysis patients as it improves the survival rates. The presence of HCV infection increases the CAN rate and the influence on allograft survival is evident at the fifth year of assessment.     

Long-term impact of hepatitis B, C virus infection on renal transplantation

Chronic liver disease and its complications are major problems in renal transplant recipients. Our aim was to elucidate the influence of hepatitis B, C virus infection on the long-term outcome of renal transplantation. Four hundred and seventy-seven patients who received renal transplantation between January 1984 and December 1999, and who were followed up at our hospital were enrolled. HBsAg was detected by the RIA method and anti-HCV Ab was assayed by the second-generation RIA kit. SGOT/ SGPT were checked every 3 months. Hepatoma was diagnosed by dynamic CT scan, elevated alpha-fetoprotein, hypervascularity by angiography and confirmed by pathological examination. The prevalence of HBV, HCV, coinfected HBV/HCV was 9.9% (n = 47), 28.5% ( n = 136), 3.1% (n = 15), respectively. The incidences of hepatoma in the HBV-/HCV-, HBV-/HCV+, HBV+/HCV-, HBV+/HCV+ groups were 1.4% (n = 4), 4.4% (n = 6), 6.4% (n = 3), 6.7% (n = 1), respectively (p = 0.114). The incidences of liver cirrhosis/hepatic failure were 3.2% (n = 9), 6.6% (n = 9), 21.3% (n = 10), 20% (n = 3), respectively (p < 0.001). The frequencies of chronic liver disease were 10.4% (n = 29), 45.6% (n = 62), 66% (n = 31), 80% (n = 12), respectively (p < 0.001). Patient and graft survival rates were lower in the HBV-infected group than in the other groups. Cox regression analysis revealed that HBV infection is likely an independent risk factor for patient mortality although the statistical significance was only borderline. Patients with HBV as well as HCV infection were not at risk of graft loss according to this model of analysis. Patients with HBV infection showed higher incidences of hepatoma, hepatic failure, graft failure and death. Therefore, HBV-infected patients who are candidates for renal transplantation should be carefully evaluated. It seems that HCV infection has little influence on the outcome of renal transplant recipients. A longer period of follow-up is needed to clarify the impact of HCV on renal transplant recipients.     

Chronic hepatitis B virus infection in renal transplant recipients

Although in Western Europe and North America the prevalence of chronic hepatitis B virus (HBV) infection has declined in patients awaiting renal transplantation, it remains a relevant clinical problem, mainly in patients with a long history of renal replacement therapy (RRT) who may have been infected many years ago. At the same time, a significant proportion of renal transplant recipients (RTR) is at risk for HBV infection in areas with endemic HBV. HBV infection may increase morbidity and mortality in RTR. The majority of long-term studies reported reduced patient survival compared with hepatitis B surface antigen (HBsAg)-negative RTR. The risk for morbidity and mortality of HBsAg-positive RTR transplantation is probably related to the extent of pretransplant liver disease. A thorough evaluation, including liver biopsy in many patients, is required to assess the individual HBsAg-positive patient's risk-benefit ratio. The influence of immunosuppressive therapy on HBV replication and HBV-associated complications is not well established and for clinical practice individually tailored immunosuppression is recommended in HBsAg-positive RTR. Careful screening for HBV reactivation in HBsAg-positive RTR and a regular clinical follow-up after renal transplantation (RTX) including liver sonography is required for early detection of HBV-associated complications. With the availability of new antiviral drugs, new options for pre- and posttransplant therapy might improve the prognosis of RTR with chronic HBV infection.     

Management of recurrence of hepatitis C infection following liver transplantation

Liver disease secondary to hepatitis C infection is the most common indication for liver transplantation. Infection of the allograft begins at the time of transplantation. The histological progression of hepatitis C infection is greatly accelerated in liver transplant recipients when compared to the natural history in immunocompetent patients. Chronic allograft injury is apparent in >50% of HCV-infected recipients in the first postoperative year. Approximately 10% of HCV-infected recipients die or lose their allograft secondary to hepatitis C-associated allograft failure and a further 30% will have cirrhosis by the end of the fifth postoperative year. Cumulative exposure to corticosteroids is associated with increased mortality, higher levels of HCV viremia and more severe histological recurrence. In contrast to non-HCV-infected recipients, treatment for acute cellular rejection is associated with attenuated patient survival among recipients with hepatitis C. Therapy with pegylated IFN (+/- ribavirin), although less efficacious than in immunocompetent patients, should be considered in recipients with histologically apparent recurrence of hepatitis C before jaundice develops. Ribavirin is poorly tolerated in liver transplant recipients, limiting efficacy of combination therapy. Ribavirin dosing should be adjusted for renal insufficiency. Passive immunity, through anti-HCV antibody preparations, has not been efficacious to date. The role of hepatitis C new immunosuppression agents in the management of posttransplant hepatitis C infection is still evolving.     

Hepatitis B and hepatitis C virus infection and outcome of hemodialysis and kidney transplant patients

AIM: A comparison of the outcome of hepatitis virus-positive and -negative kidney transplant and hemodialysis patients was the aim of this investigation. MATERIALS AND METHODS: The study involved 384 kidney transplant patients (67 HBsAg positive, 39 anti-HCV positive, 278 hepatitis negative), transplanted between 1987 and 2001, and 403 hemodialysis patients (128 HBsAg positive, 83 anti-HCV positive, 192 hepatitis negative) who had started hemodialysis and were referred to the kidney transplant waiting list during the same period. RESULTS: Hemodialysis patients were older than transplant patients. Comparison of the groups' survival rates, adjusted for patient age, showed that all kidney transplant patients survived longer than hemodialysis patients (p < 0.001). HBV infection had a negative impact on patient survival, especially in hemodialysis patients. HCV infection did not have a significant influence on patient survival. Cardiovascular disease was the main cause of death of all hemodialysis- and hepatitis-negative transplant patients. Liver failure was one of the leading causes of death in HBV-positive transplant patients. Mortality risk was higher for older patients, HBV-positive and -negative hemodialysis patients. CONCLUSIONS: Kidney transplantation offers longer survival for hepatitis-positive and -negative hemodialysis patients. HBV but not HCV infection had a negative impact on ESRD patient survival.     

The clinical outcome of hepatitis C virus antibody-positive renal allograft recipients.

In order to investigate the prevalence of antibody to hepatitis C virus (anti-HCV) in renal transplant patients, the evolution of anti-HCV status, and clinical outcome in anti-HCV-positive renal allograft recipients, we tested the sera from 120 renal transplant patients for anti-HCV. Thirty-eight patients were hepatitis B surface antigen (HBsAg)-positive. Two patients were anti-delta-positive. A total of 79 patients (65.8%) had at least one serum positive for anti-HCV. Anti-HCV positivity decreased after transplantation for more than 5 years (65.5% at transplantation versus 37.9%, 78.3 +/- 13.4 months later). Among those with positive anti-HCV, the HBsAg-positive group had significantly higher incidence of chronic hepatitis (50% vs. 25.5%, P = 0.026) and liver cirrhosis (21.4% vs. 0%, P = 0.001) than HBsAg-negative group. Among the 82 HBsAg-negative patients, the prevalence of anti-HCV was significantly higher in those with chronic hepatitis than in those without (86.7% vs. 56.7%, P = 0.027). We conclude from this study: (1) anti-HCV positivity is quite prevalent in renal transplant patients; (2) coinfection of hepatitis B virus (HBV) and hepatitis C virus (HCV) may lead to aggressive liver disease and cirrhosis; HCV infection alone has a more benign clinical outcome; and (3) HCV infection is an important cause of posttransplant chronic hepatitis in HBsAg-negative patients.     

Impact of hepatitis B and C on graft loss and mortality of patients after kidney transplantation

BACKGROUND: Mortality or graft loss after renal transplantation might be influenced by hepatitis virus infection. METHODS: Sera from time of transplantation of 927 renal transplant recipients were tested for hepatitis C (HCV) and hepatitis B virus (HBV) in order to investigate the impact of hepatitis virus infection on graft loss and mortality over an observation period of 20 yr. RESULTS: One hundred and twenty three of 927 patients were HCV positive, 30 patients HBV positive and seven patients HBV and HCV positive. The observation period was 9.2 +/- 4.4 yr. Mortality was significantly higher in patients with hepatitis B (p = 0.0005), as well as in patients with concomitant B and C hepatitis (p < 0.0001) and in those who acquired HCV infection after transplantation (n = 30, p = 0.0192) compared with non-infected patients. Patients with replicating HBV infection (HBeAg positive) had the worst prognosis (p < 0.0001). In the multivariate analysis the presence of HBeAg (p < 0.0001), patients' age (p < 0.0001) and HCV infection after transplantation (p = 0.0453) were predictors for death. Graft survival was significantly shorter in patients with concomitant hepatitis B and C (p = 0.0087) as well as in HBeAg positive patients (p = 0.002). HCV infection or HBs antigenemia did not have a significant impact on graft survival compared with non-infected patients. CONCLUSION: HCV infection after transplantation is associated with a high mortality whereas chronic HCV infection before trans plantation does not have a significant impact on mortality. Patients with replicating HBV infection or concomitant HBV and HCV infection have a high risk of graft loss and mortality.     

Hepatitis B disease in dialysis and transplant patients. Further epidemiologic and serologic studies

As hepatitis B virus (HBV) infection in renal transplant recipients is associated with a high incidence of progressive liver disease it may be inadvisable to transplant hemodialysis patients with hepatitis B antigenemia. To determine the natural history of HBV disease in hemodialysis patients, all 49 patients on hemodialysis treatment for at least 1 year, at 3 centers, who developed circulating hepatitis B surface antigen (HBsAG), were studied. A subgroup of these patients (n = 31) aged less than or equal to 50 years, followed for 55 +/- 6 months after detection of HBsAg was compared with 22 previously studied HBsAg-positive transplant patients followed for 81 +/- 9 months. Significantly more transplant patients developed chronic hepatitis defined biochemically (P less than .001) and none of the transplant patients became HBsAg-negative compared with 19% of the hemodialysis group. Taking difference in follow-up into account, mortality was significantly higher in the transplant recipients (P less than .005) following development of HBsAg antigenemia, and the mortality difference was attributable to deaths from liver disease. A total of 36 serum samples from 14 of the 22 HBsAg-positive renal transplant recipients was analyzed for hepatitis B e antigen (HBeAg), antibody to hepatitis D virus (anti-HD), and hepatitis B virus deoxyribonucleic acid (HBVDNA) concentration. No serum sample was anti-HD-positive. Twelve of the 14 patients were HBeAg-positive. Five patients became HBeAg-negative, 3 of whom developed aggressive liver disease. One HBeAg-negative anti-HBe-positive patient had progression of liver disease from asymptomatic carrier status to chronic active hepatitis (CAH). Of 14 patients, 9 developed progressive CAH. HBVDNA concentration was not diagnostic of disease activity on liver biopsy. However only 1 sample of 10 measured in 5 patients with nonprogressive disease had a level greater than 100 pg/L, compared with 9 of 17 in the group who progressed to CAH. During the interval when the liver histology progressed from asymptomatic carriage or chronic persistent hepatitis (CPH) to CAH, the HBVDNA concentration increased by greater than 10 times baseline in 4 of 5 patients who had serial samples, whereas this did not occur in 4 patients with nonprogressive disease. We conclude that the long-term outcome of hepatitis B infection in transplant recipients is significantly worse than in hemodialysis patients. Therefore it may be inadvisable to transplant HBsAg-positive hemodialysis patients.(ABSTRACT TRUNCATED AT 400 WORDS)     

Outcomes of Kidney Transplantation Recipients With Hepatitis in the Antiviral Therapy Era: A Single-Center Experience

Introduction

The use of organs from hepatitis B surface antigen (HBsAg)+ donors could increase the donor pool substantially. However, fulminant hepatic failure requiring urgent liver transplantation or resulting in death has been reported in recipients of HBsAg+ renal transplantation (KT) in pre-nucleos(t)ide analog (NA) era. With effective antiviral therapies such as NAs, it seems feasible to transplant such recipients more safely. To address this issue, we conducted a retrospective, cohort study to evaluate the safety and long-term risks of HBsAg+ KT recipients in the NA era.

Methods

From December 2006 to January 2013, 112 patients undergoing KT were followed at our institute. We analyzed patient and graft outcomes, hepatitis status (HBsAg status, hepatitis B virus [HBV] DNA level, liver function tests, presence of hepatitis C virus [HCV] co-infection), and graft source (domestic or transplant tourism).

Results

Ninety-two KT recipients were still alive. Nine patients were died of nonhepatic factors. Among 112 patients, there were 19 of 92 recipients alive who were HBsAg+, including 6 patients with HBV and HCV dual infections. Two of 19 patients experienced symptomatic hepatitis, one de novo and the other re-activation. Liver functions of these 2 recipients recovered progressively after introduction of NAs. No recipients in our study had experienced graft loss at the time of analysis.

Conclusion

In terms of patient survival and quality of life, KT seems be a safe and feasible therapy of choice for HBsAg+ patients with end-stage renal disease. Infection is easier to prevent than to treat. KT recipients at high risk for HBV reactivation and for complications of HBV, with or without HCV co-infection, may benefit from longer prophylaxis. However, the optimal duration of prophylaxis remains unclear. Furthermore, several issues needed to be solved for clinical concerns, such as frequency and intensity of adverse effects, high costs, increased pill burden, drug–drug interactions, and the emergence of viral resistance variants.     

Transplanting kidneys from donors with prior hepatitis B infection: one response to the organ shortage

While the number of cadaveric organ donors remains relatively stable, the number of patients awaiting transplantation continues to increase, creating a shortage of donor organs. To address this imbalance, there is interest in transplanting organs formerly considered marginal or undesirable. Thus, more organs are currently transplanted from living donors, older donors, hemodynamically unstable donors, non-heart-beating donors and donors with markers of prior hepatitis B virus (HBV) infection. A large number (up to 93.8%) of liver transplant seronegative recipients from anti-HBc antibody positive donors have acquired HBsAg after liver transplantation in the absence of immunoprophylaxis. Based on experience in liver transplantation programs, transmission of HBV from donors without HBsAg but with antibody to HBV core antigen (anti-HBc), although conventionally defined as evidence of resolved infection, can have adverse consequences on both graft and recipient. On the contrary, HBV appears to be in-frequently transmitted from HBsAg negative/anti-HBcAb positive kidney donors: the incidence of de novo HBsAg seropositivity after renal transplantation ranges between 0 and 5.2%. A significantly higher incidence of anti-HBc antibody seroconversion (without developing HBsAg) after renal transplantation with anti-HBc antibody positive donors was seen. However, anti-HBc antibody positive renal allografts should be considered, especially for recipients who have been successfully immunized with HBV vaccine. Prospective long-term studies are in progress to assess the risk of de novo HBV infection (HBsAg seroconversion) in renal transplant recipients who have not been successfully immunized with vaccine against HBV.     

Clinical course of hepatitis C virus infection in renal transplant recipients

Patients with end-stage renal disease are at high risk for exposure to hepatitis C virus (HCV) infection. Although both viral replication and liver disease progression are accelerated after renal transplantation, the long-term impact of chronic HCV infection is unclear. Our aim was to analyze the course of HCV infection in renal transplant recipients and the effects of HCV reactivation on patient and graft survival. METHODS: We retrospectively examined the 21-year (1985-2006) data of 1274 renal transplant recipients, 43 of whom were anti-HCV positive at the time of transplantation. RESULTS: The mean posttransplant follow-up of 43 patients was 62.0 +/- 7.3 months. At the time of transplantation, HCV RNA was positive in 11 (25.6%) patients and negative in 32 (74.4%) patients. HCV reactivation was seen in 19 (45.2%) patients at a mean time of 20.8 +/- 5.7 months. In 31 (72%) patients, acute rejection occurred, whereas graft loss occurred in 10 (23%) patients. Three (7%) patients died. Among 43 patients, 22 (51.2%) were treated with interferon before transplantation. There was a statistically significant association between pretransplant interferon therapy and pretransplant HCVRNA level (P=.024), but no significant association of HCV reactivation and graft rejection, mortality, or kidney survival. CONCLUSION: HCV reactivation occurred in nearly half of the renal transplant recipients, mostly in the second year. Patient survival and graft survival were not affected by HCV reactivation. Anti-HCV positivity should not preclude chronic renal failure patients from renal transplantation.     

A role for chronic parvovirus B19 infection in liver dysfunction in renal transplant recipients?

BACKGROUND: Clinically, liver dysfunction in renal transplant recipients is related to hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. The contribution of parvovirus B19 (B19) to liver disease in renal transplant recipients has not been studied. Here we present the association of liver dysfunction with or without the coinfection of B19, HBV, and HCV after renal transplantation. METHODS: We used enzyme-linked immunosorbent assay to identify B19, HBV, and HCV infections in serum samples taken from 144 renal transplant recipients before transplantation and at 12 and 24 months after transplantation. After each patient had fasted for 12 hr, blood was taken for measurement of aspartate aminotransferase and alanine aminotransferase monthly for at least 6 months. RESULTS: Liver dysfunction developed at the significantly higher incidence of 47% in the anti-HCV(+) patients compared with 6% in the noninfected group (P<0.0001). HBV infection had no impact on the incidence of liver dysfunction in renal transplant recipients. A higher incidence of liver dysfunction was found in 42% of B19 IgG(+)IgM(-) group patients compared with 13% of the B19 IgG(+)IgM(+) group (P=0.0051) and 9.5% of the B19 IgG(-)IgM(-) group (P=0.0003). A B19 polymerase chain reaction (PCR) assay revealed significantly higher liver dysfunction in 29% of B19 PCR(+) group patients compared with 13.6% of B19 PCR(-) patients (P=0.0419). Patients who were anti-HCV(+) and B19 PCR(+) had a significantly higher incidence of liver dysfunction than B19 PCR(-) patients (P=0.002). CONCLUSIONS: Chronic B19 infection and HCV infection, both separately and in combination, increase the incidence of liver dysfunction in renal transplant recipients. HBV infection does not seem to be independently or synergistically associated with liver dysfunction.     

Hepatitis B and Hepatitis C Virus Infection and Outcome of Hemodialysis and Kidney Transplant Patients

Aim. A comparison of the outcome of hepatitis virus-positive and -negative kidney transplant and hemodialysis patients was the aim of this investigation. Materials and Methods. The study involved 384 kidney transplant patients (67 HBsAg positive, 39 anti-HCV positive, 278 hepatitis negative), transplanted between 1987 and 2001, and 403 hemodialysis patients (128 HBsAg positive, 83 anti-HCV positive, 192 hepatitis negative) who had started hemodialysis and were referred to the kidney transplant waiting list during the same period. Results. Hemodialysis patients were older than transplant patients. Comparison of the groups’ survival rates, adjusted for patient age, showed that all kidney transplant patients survived longer than hemodialysis patients (p < 0.001). HBV infection had a negative impact on patient survival, especially in hemodialysis patients. HCV infection did not have a significant influence on patient survival. Cardiovascular disease was the main cause of death of all hemodialysis- and hepatitis-negative transplant patients. Liver failure was one of the leading causes of death in HBV-positive transplant patients. Mortality risk was higher for older patients, HBV-positive and -negative hemodialysis patients. Conclusions. Kidney transplantation offers longer survival for hepatitis-positive and -negative hemodialysis patients. HBV but not HCV infection had a negative impact on ESRD patient survival.     

Severe clinical course of de novo hepatitis B infection after liver transplantation.

The aim of this study is to determine the origin, clinical outcome, allograft histological characteristics, and virological outcome of de novo hepatitis B virus (HBV) infection after orthotopic liver transplantation (OLT). We studied 136 hepatitis B surface antigen (HBsAg)-negative liver transplant recipients. HBV DNA was detected by dot-blot hybridization and polymerase chain reaction (PCR). The S gene was sequenced. Hepatitis C virus (HCV) RNA was assessed by PCR. The long-term clinical and histological outcome was determined. Six of 136 HBsAg-negative patients (4.4%) became HBsAg positive after transplantation. The source of HBV infection was reactivation of latent HBV infection in 2 patients and was not identified in 4 patients. Two donors had isolated core antibody. Two of these 6 patients developed acute liver failure related to hepatitis B. The 4 other patients had severe chronic hepatitis related to hepatitis B. All patients had high-level HBV replication. No significant mutations in the S gene were found. These data suggest that de novo hepatitis B infection is not a mild disease and might represent a significant cause of graft dysfunction. This is the first report of fulminant hepatitis caused by de novo hepatitis B infection after OLT.     

Hepatocellular carcinoma after renal transplantation: the long-term impact of cirrhosis on chronic hepatitis B virus infection

Hepatocellular carcinoma (HCC) is the most common posttransplantation malignancy in hepatitis B virus (HBV) endemic areas. The aim of this study was to review the significant effect of liver cirrhosis on the outcome of renal allograft recipients with chronic hepatitis B. We performed a retrograde analysis of the clinical presentations of 66 hepatitis B surface antigen-positive kidney allograft recipients during the past 25 years with a mean follow-up of 76 months. Seven patients were diagnosed with HCC. The patients were subgrouped into cirrhotic versus noncirrhotic liver cohorts. Among renal allograft recipients with HBV infection, patients with cirrhotic livers had a higher risk of HCC (P = .003) and mortality (P = .025) than those with a noncirrhotic liver. The outcome was poor among the cirrhotic liver group. Pretransplantation liver biopsy may be indicated for the recipient candidate with HBV infection. Liver cirrhosis may be an exclusion criterion for the renal transplant waiting list due to the high incidence of HCC and the poor patient survival.     

Hepatitis B liver disease in cyclosporine-treated renal allograft recipients

To establish the impact of cyclosporine on the development of chronic hepatitis in hepatitis B surface antigen (HBsAg)-positive renal allograft recipients, the incidence and outcome of chronic hepatitis in 20 cyclosporine-treated patients (CsA group) were compared with 13 azathioprine-treated patients (AZA group). All 33 patients had a functioning graft for 2 years or longer. Twenty-nine of the 33 patients were HBsAg-positive prior to the initiation of hemodialysis. The difference in the incidence of chronic hepatitis between these 2 groups was not statistically significant (78.6% in the AZA group vs. 52.4% in the CsA group, P = 0.12). In the CsA group, 3 patients (15%) developed liver cirrhosis, and there was a 5% mortality. The AZA group had a 7.7% mortality, and 4 patients (30.8%) developed liver cirrhosis. Serial serum samples obtained from these 33 HBsAg-positive renal allograft recipients were analyzed for antibody to hepatitis D virus (anti-HD). Anti-HD was found in 3 patients. Two of them developed anti-HD seroconversion after renal transplantation during a mean follow-up of 4 years. All 3 patients developed chronic hepatitis and 2 of them have subsequently developed liver cirrhosis. There was a mortality of 6.1% in 33 HBsAg-positive patients compared with a 5.3% mortality in 57 HBsAg-negative renal allograft recipients. The difference was not statistically significant. We conclude from this study that (1) CsA-treated HBsAg-positive renal allograft recipients have a tendency to develop chronic hepatitis like AZA-treated patients; (2) HBsAg-positive patients have an increased risk of HDV superinfection after renal transplantation, and this may result in rapid progression to liver cirrhosis; (3) HBsAg-positive patients who acquire HBsAg prior to renal transplantation have a low overall mortality, including death due to liver disease, for a mean follow-up of 4 years.     

Kidney Transplantation from Hepatitis B Surface Antigen Positive Donors into Hepatitis B Surface Antibody Positive Recipients: A Prospective Nonrandomized Controlled Study from a Single Center

The number of patients on renal transplant waiting list is increasing rapidly in many countries, exacerbating the shortage of organs. We conducted a study to evaluate the safety and efficacy of deceased-donor kidney transplantation from hepatitis B surface antigen (HBsAg)-positive (+) donors into hepatitis B surface antibody (anti-HBs)-positive (+) recipients. Sixty-five patients received grafts from HBsAg(+) donors, and 308 subjects received grafts from HBsAg-negative(−) donors. Posttransplantation, recipients with HBsAg(−) grafts or HBsAg(+) grafts received 400 U of hepatitis B immunoglobulin once and twice, respectively. The seven recipients who received grafts from hepatitis B virus (HBV) DNA(+) donors were treated with hepatitis B immunoglobulin 400 U weekly for 3 months and lamivudine 100 mg daily for 6 months. All patients were monitored for liver function and hepatitis B viral status. The follow-up period was 38.7 ± 15.4 months. Although two recipients developed de novo HBV infection, neither patient developed severe liver dysfunction nor died. The incidence of liver injury (39/65 vs. 207/308, chi-square test, p > 0.05) and survival (log-rank test, p > 0.05) did not differ between the groups. We conclude that anti-HBs(+) recipients receiving HBsAg(+) grafts did as well as those receiving HBsAg(−) grafts.