Review article: Hepatitis B and dialysis


Professor David Johnson, Department of Nephrology, Level 2, ARTS Building, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane, Qld 4102, Australia.


The incidence of hepatitis B virus (HBV) infection in dialysis populations has declined over recent decades, largely because of improvements in infection control and widespread implementation of HBV vaccination. Regardless, outbreaks of infection continue to occur in dialysis units, and prevalence rates remain unacceptably high. For a variety of reasons, dialysis patients are at increased risk of acquiring HBV. They also demonstrate different disease manifestations compared with healthy individuals and are more likely to progress to chronic carriage. This paper will review the epidemiology, modes of transmission and diagnosis of HBV in this population. Prevention and treatment will be discussed, with a specific focus on strategies to improve vaccination response, new therapeutic options and selection of patients for therapy.

Hepatitis B virus (HBV) infection is a substantial global health problem. It is estimated that more than two billion people worldwide have serological evidence of current or historical infection.1 HBV is highly infectious compared with other blood-borne viruses: An untreated percutaneous exposure to an infected source carries a risk of seroconversion of up to 30%. By contrast, the risks for hepatitis C virus and human immunodeficiency virus (HIV) are 1.8% and 0.31%, respectively.2 Acute infection occasionally results in fulminant hepatitis, but more importantly can progress to a chronic state, where decompensation, cirrhosis and hepatocellular carcinoma are all potential complications. Compared with the general population, dialysis patients are at increased risk of acquiring HBV. Reasons include increased exposure to blood products, shared haemodialysis (HD) equipment, breaching of skin and immunodeficiency. Haemodialysis, which requires access to the bloodstream, also affords an opportunity for transmission of HBV between patients, and between patients and staff. Viral hepatitis complicating HD has been recognized from the earliest days of this therapy. While the introduction of vaccination programmes and stringent infection control measures have succeeded in limiting the spread of hepatitis infection within dialysis facilities, outbreaks continue to occur periodically and prevalence rates remain unacceptably high. As such, HBV infection remains an important issue in renal replacement therapy.


Hepatitis B is a blood-borne virus. Modes of infection include perinatal, and through percutaneous or mucosal exposure to infected blood or body fluids.3

There are considered to be more than 350 million people worldwide with chronic hepatitis B infection.4 More than 75% of these live in the Asia–Pacific region, with high numbers also residing in Africa and the Amazon basin. In areas of high endemicity, the lifetime infection rate is above 50%, and more than 8% of the population are chronic carriers.5 Infection in such regions is typically acquired in childhood, either horizontally from other children or perinatally from maternal carriers. By contrast, parenteral transmission is common in Australia, and fewer than 2% of the population are chronic HBV carriers.

Hepatocellular carcinoma is the sixth most common cancer worldwide, and half of all cases are caused by HBV.6 HBV is the second most important carcinogen after cigarette smoke.

In dialysis units both patient-to-patient and patient-to-staff transmission of the virus have been recognized since the 1960s. Before the advent of vaccination, some success in limiting the spread of HBV was achieved by dialysing seropositive patients separately from those who were seronegative. This followed the publication in the UK of the Rosenheim Report in 1972,7 which set out a code of practice for reducing transmission of hepatitis among dialysis patients. In 1977, guidelines were published in the USA to reduce HBV infection in dialysis units.8 The incidence of new hepatitis B infections in US dialysis patients subsequently fell from 6.2% in 1974 to 1% by 1980.9 Testing of a vaccine began in the 1970s, and this came into widespread clinical use from the early 1980s.10,11 This further reduced the risk of HBV infection in the dialysis setting.

Nevertheless, although rates of new infection are now low,12 hepatitis B continues to exist in dialysis populations. Prevalence rates tend to be dependent on baseline population rates. An analysis of data from the Dialysis Outcomes and Practice Patterns Study showed an HBV prevalence of 0–6.6% across dialysis facilities in Western Europe, Japan and the USA.13 In contrast, a registry study of Asia–Pacific countries found the prevalence of hepatitis B surface antigen (HBsAg) positivity ranged between 1.3% and 14.6%.14 Reports from much smaller cohorts elsewhere have indicated HBsAg positivity rates of 13.3% in Turkey, and 2.4–10% in Brazil.15–17

In addition to being at increased risk of infection, it has been demonstrated that HD patients are more likely to become chronic carriers of HBV than members of the general population.18


Patients with chronic kidney disease (CKD) have impaired host defences against viral infections.19 Consequently, risk of acquisition is increased in dialysis populations regardless of dialysis modality. Before the introduction of erythropoietin therapy, CKD patients were also at increased risk of infection via transfusion of contaminated blood products.

The HD procedure presents the opportunity for blood contact with contaminated equipment, injection of liquids harbouring virus, and exposure of broken skin or mucous membranes to infection. HBV is particularly persistent in the environment, and may survive for more than a week on surrounding surfaces.20 Moreover, dialysis patients are more likely to be hospitalized, and to require interventional procedures or surgery.21

Historically, groups of patients in early peritoneal dialysis (PD) programmes were dialysed incentre using intermittent PD. Because PD effluent from HBsAg positive patients is potentially infectious,22 this regular gathering of patients facilitated transmission of HBV. As a consequence, early infection risks were similar for PD and HD.23 With the development of PD as a predominantly home therapy, rates of HBV infection in this population have fallen, so that the prevalence of HBV in PD populations is now heavily influenced by the underlying population prevalence. In countries with very high endemicity of HBV, both PD and HD programmes have similar rates of seropositivity, reflecting HBV acquired before the commencement of dialysis.24,25 Conversely, in countries with low background prevalence, present-day risk of HBV in PD patients is associated with exposure to blood products and previous time spent on HD.

The latest US guidelines for HBV infection control in dialysis units were published in 2001.26,27 Other countries have also produced guidelines.28–30 Underpinning these are established infection-control principles. These include vaccination and screening of HD patients, and segregation of those that are infectious. Safe sharp handling is advised, as is avoidance of multidose vials for intravenous drugs. Other developments that have contributed to a reduction in infection risk include a widespread move from reusable membranes towards disposable dialysers and the introduction of synthetic erythropoietin with a decrease in blood transfusion.

Dialysis unit staff members are at risk of infection through exposure during the dialysis procedure. Infection with HBV compromises their own health, and risks further staff-to-patient transmission of HBV. Vaccination of all dialysis unit staff is recommended by guidelines, and response rates are >90%.31 Non-responders who are HBsAg positive should be counselled and assessed accordingly, those who are HBsAg negative should be warned to seek post-exposure prophylaxis in the event of contact with potentially infectious blood. Other steps that can be taken to prevent cross infection with HBV between patients and staff include barrier protection, such as wearing gloves and face shields. Cleaning hands and changing gloves between contacts prevents staff infecting one patient from another. Minimizing staff turnover and allocating dedicated staff to infectious patients is important. Full guidelines relating to management of occupational exposure to HBV, including needlestick injuries is available from the Centers for Disease Control.32

Despite the successes of these measures, HBV outbreaks continue to occur intermittently in HD units. These do not point to inadequacies in infection-control guidelines, but rather to shortcomings in following such recommendations. In a review of 30 nosocomial HBV outbreaks since 1992, 10 occurred in a HD setting.33 The most common transmission pathways for these infections were multi-use drug vials (30.3%) and non-disposable capillary blood sampling devices (27.3%). An analysis of five HBV outbreaks in the USA during 1994 found that patients were infected through failures of isolation, serological screening and vaccination, and through sharing of staff, equipment and supplies between patients.34


Commonly used serological tests for HBV include those for HBsAg, antibody to HBsAg (anti-HBs), antibody to hepatitis B core antigen (anti-HBc) and viral DNA (HBV DNA) by polymerase chain reaction (Table 1).

Table 1.  Significance of HBV serologic tests
Serological markerSignificance of positive test
  1. Anti-HBc, antibody to hepatitis B core antigen; anti-HBs, antibody to hepatitis B surface antigen; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus.

HBsAgPresent in acute or chronic infection. Indicates the patient is infectious. Sometimes transiently detected after vaccination.
HBeAgPresent in acute or chronic infection. Indicates ongoing viral replication. A surrogate marker for high HBV DNA levels.
Anti-HBsPresent after successful recovery from hepatitis B infection. Also present after successful vaccination. Indicates immunity.
Anti-HBcAppears shortly after HBsAg in acute infection. Indicates previous or current HBV infection.

In primary infection, there is an incubation period of 4–10 weeks duration, following which HBsAg appears in blood. Anti-HBc antibodies appear soon afterwards. In the acute phase, anti-HBc antibodies are principally of the immunoglobulin M class.35 HBV DNA levels are high from very early in acute infection. Usually the e antigen is detectable in the bloodstream a short time after anti-HBc becomes apparent.36 HBV DNA and hepatitis B e antigen (HBeAg) usually disappear before the clearance of HBsAg, which happens after 1–2 months. Anti-HBs antibodies are present from several weeks after the disappearance of HBsAg, and anti-HBc antibodies persist indefinitely, switching to IgG after 6–24 months. The detection of anti-HBc and anti-HBs signifies previous infection.37 Anti-HBs antibodies at a titre of >10 IU/L indicate immunity.

In a proportion of patients infected by HBV, chronic infection supervenes. Persistence is seen in 90% of perinatally infected infants, 20–30% of children infected between 1 and 5 years of age, 6% of those infected between 5 and 15 years old, and only 1–5% of adults.4 An ‘immune-tolerant’ phase of chronic infection is typically seen in those infected as infants or children. There may be a brief ‘immune-tolerant’ phase in infected adults, but this is uncommon. During this period, HBsAg, HBeAg and HBV DNA are detectable, and the patient is usually asymptomatic, with normal transaminases and liver histology.38

Following this period, or immediately in adult infection, is an ‘immune-clearance’ phase. This is characterized by intermittent surges in serum transaminase levels, and may occasionally be accompanied by hepatic decompensation. Cirrhosis can develop as a consequence, but usually this phase culminates in the clearance of HBeAg and seroconversion to anti-HBe. HBV DNA falls to low levels (<2000 IU/L) and may disappear altogether, while HBsAg persists.39

There is a third ‘inactive residual’ phase during which HBV DNA levels remain low and a low rate of HBsAg seroclearance is seen (between 1–2% annually).40,41 Where HBsAg seroclearance occurs, and provided cirrhosis has not supervened, the prognosis is usually excellent. Occasionally, an ‘occult infection’ state remains in which HBsAg is undetectable, and anti-HBc is usually measurable, but a small quantity of HBV DNA persists. It is possible that patients in this state are infectious despite the negative HBsAg.42

Reports of transient HBsAg seropositivity after vaccination exist. Most likely this is vaccine-induced, spurious, and persists for up to 20 days.43 No action is required assuming the HBsAg serology is negative once again after 3 weeks.


The hepatitis B vaccine

In the 1970s, Krugman observed that HBsAg was immunogenic, and that anti-HBs antibodies were protective against hepatitis B.44 A first-generation vaccine was subsequently developed, consisting of HBsAg extracted by plasmapheresis from HBV carriers, and then inactivated.45 This vaccine, manufactured by Merck, was approved by the Food and Drug Administration in 1981, and became widely available from July 1982. A similar vaccine was licensed at about the same time, produced by Institut Pasteur in France.

Modern ‘second-generation’ HBV vaccines are recombinant non-infectious subunit vaccines containing HBsAg.46 These are produced by the yeast Saccharomyces cerevisiae using recombinant DNA technology. There are two such HBV vaccine formulations available, Engerix B and Recombivax HB.

A third-generation vaccine has been produced from a mammalian cell line, although it is not yet in widespread use. It contains the pre-S1 and pre-S2 antigens that are present on the viral envelope. These antigens are more immunogenic than the HBsAg present in second-generation vaccines.47

Whichever vaccine is used, providing manufacturer's recommendations are adhered to, immunogenicity and efficacy are considered equivalent.48 In line with Krugman's earlier observations, efficacy studies have shown that at least 90% of subjects developing anti-HBs levels of 10 IU/L are protected from hepatitis B infection.49 Safety data are comprehensive. A large prospective trial has shown the vaccine to be safe and well-tolerated.50

Efficacy of hepatitis B vaccine

Szmuness et al.51 demonstrated the efficacy of the first-generation, plasma-derived HBV vaccine (PDV) in 1980 in a randomized, double-blind placebo-controlled trial (RCT) in a high-risk population with normal renal function. The same group then investigated use of the Merck vaccine in 79 US HD patients and demonstrated that 89% produced detectable anti-HBs.10

The Pasteur vaccine was examined in an RCT of 138 dialysis patients. Despite a low seroconversion rate of 60%, the vaccine was protective when compared with placebo (Table 2).52 Another observational study of the Merck vaccine found seroconversion rates of 50% in male HD patients and 66% in females. By contrast, 100% of seven pre-dialysis patients had protective antibody.53 Szmuness' group reported the largest RCT of HD patients in 1984 (n = 1311).54 A three-dose schedule produced a 50% response rate. Two other early studies found seroconversion rates in HD patients of 60–75%.11,55 The second, a Dutch RCT, replicated the findings of the prior French study,52 showing that the vaccine was protective against HBV infection compared with placebo.

Table 2.  Studies of first-generation hepatitis B vaccines and seroconversion rates
StudyVaccine dose and scheduleNo. of haemodialysis patients fully vaccinatedSeroconversion rate (%)
Stevens et al.1240 µg × 3 or 47989
Months 0, 1, (2), 6
Crosnier et al.525 µg × 34360
Months 0, 1, 2
Desmyter et al.133 µg × 417075
Months 0, 1, 2, 5
Stevens et al.5440 µg × 356250.3
Months 0, 1, 6
Köhler et al.5340 µg × 310350
Months 0, 1, 6

The overall message from all these trials of HBV vaccine in HD patients was that HD patients were substantially less responsive to the vaccine than healthy individuals, but that the vaccine did confer protection from HBV infection. There was a suggestion that women responded better than men to vaccination.

The second-generation or yeast-derived vaccine (YDV) was found to have similar efficacy in healthy recipients to the earlier PDV. An early investigation found 97% seroconversion in 32 HD patients with the YDV.56 Bruguera et al. examined the YDV in over 270 HD patients.57 Using a four-dose schedule and dosing at 0, 1, 2 and 6 months with 40 µg vaccine, 69% of patients achieved an anti-HBs titre of ≥10 IU/L (considered protective). If the fourth dose was given at 12 months, the seroprotection rate reached 76%.

Strategies for improving immune response

When the vaccine is used in immunocompetent individuals using a three-dose schedule, a 90–95% seroprotection rate is expected. Clearly, in vaccine recipients with renal failure, the rates are substantially lower. In an attempt to improve seroconversion rates, current recommendations state that dialysis patients should receive higher vaccine doses than individuals with normal renal function. As such, 40 µg of Recombivax HB at 0, 1 and 6 months, or 40 µg of Engerix B at 0, 1, 2 and 6 months should be administered. The best reported response rates to these schedules are <85% achieving seroprotection.58,59

Not only is the response to the vaccine blunted, but anti-HBs levels decline more rapidly after immunization in HD patients compared with healthy individuals, such that in 41% of responsive patients the levels are undetectable at three years.60 Other reports suggest that in up to 42% there are no detectable anti-HBs levels one year after vaccination.26

The likelihood of a seroconversion response to hepatitis B vaccine decreases as renal failure progresses. As mentioned above, Köhler et al. found a far superior response to the PDV in their small group of pre-dialysis patients.53 This has been borne out by other studies more recently using YDV.61,62 As a result, guidelines also recommended that patients with CKD be vaccinated as early as possible in the course of their renal disease. Although vaccinating patients before dialysis makes immunological sense, there are substantial cost implications in vaccinating much larger numbers of patients: Many pre-dialysis patients will never progress to renal replacement therapy, succumbing instead to their comorbidities.

Vaccine adjuvants have been studied in HD patients. The addition of granulocyte-macrophage colony-stimulating factor and interleukin-2 has not been consistently successful in improving response rates.63,64 Likewise, studies have failed to show a significant, durable benefit of interferons or thymopentin.65–67 Alternatively, a more recent vaccine formulation (HBV-AS04) consisting of standard Engerix B YDV with adjuvant 3-O-desacyl-40-monophosphoryl lipid A, has shown the ability to provide earlier and greater anti-HBs responses than the standard vaccine.68 More importantly, a small follow-up study has shown that the rate of decline in seroprotectivity was slower for the HBV-AS04 vaccine.69 As such, this is the most promising vaccine adjuvant to date. It was licensed for use in CKD patients in Europe in 2005.

Finally, studies have investigated whether intradermal (ID) vaccination may afford improved seroconversion. HBV vaccination in healthcare workers was evaluated in a Cochrane review in 2005.70 Low-dose ID injection was shown to provide lower anti-HBs levels than high-dose intramuscular (IM) vaccination in this immunocompetent group of recipients. The following year a meta-analysis of IM versus ID vaccination in HD patients concluded that the ID route generated a superior anti-HBs response at the end of the vaccination protocol, but no significant differences in antibody levels were seen over longer follow-up.71 A similar conclusion was reached from a single, small study of 60 chronic ambulatory peritoneal dialysis patients who were randomized to ID or IM vaccination.72 The peak anti-HBs titres were reached earlier in the ID group, and a higher seroconversion rate attained, but there was no difference between the two groups in maintenance of seroprotective anti-HBs levels over 2 years of follow-up. The ID route is more technically challenging and causes an increased incidence of local reactions. Given that the majority of dialysis patients will respond to primary IM vaccination, the deltoid IM route seems preferable for primary vaccination, with the ID route reserved for the more troublesome group of non-responders.

The antibody response to hepatitis B vaccination declines with time. It is current practice to administer booster doses to those with an adequate initial response whose anti-HBs levels fall below 10 IU/L. For those who do not respond adequately to the initial vaccination course, a revaccination schedule may be employed. Bock et al. assessed the effect of a shorter revaccination course of injections in a small group of HD patients.73 In this randomized controlled trial, no improved efficacy for a shorter revaccination schedule was demonstrated. By contrast Barraclough et al. used eight weekly ID injections of low-dose HBV vaccine in patients initially unresponsive to a standard vaccination schedule.74 In a randomized comparison with a 2-dose, 8-week IM vaccination schedule, the patients receiving ID vaccination had a significantly greater seroconversion rate, with a trend towards longer seroprotection in responders. The ID injections were well-tolerated. The findings were consistent with a prospective, randomized study from Italy in 1997.75 Alternatively, a small observational study from Israel found that the use of the third-generation vaccine Bio-Hep-B in a revaccination protocol yielded seroprotective anti-HBs levels in 25 of 29 initial non-responders (86%) to a standard vaccination schedule.76

Patients should therefore be vaccinated according to guidelines, with the recommended ‘double dose’ of 40 µg. If there is no response, a second series can be given. If the initial response is adequate, but anti-HBs levels fall to <10 IU/L, a booster dose should be given. Those who do not produce protective levels (≥10 IU/L) of anti-HBs after two series might be considered for ID vaccination, or the third-generation vaccine.


Drugs available for HBV infection

Available therapeutic options include interferons, the nucleoside analogues lamivudine and telbivudine, and the nucleotide analogues adefovir, tenofovir and entecavir. Interferon-α was the first available therapy for chronic HBV infection. Experience in dialysis patients comes from treatment of hepatitis C. In this group, it has been shown that renal failure greatly increases the half-life and area under the concentration–time curve.77 Side effects are therefore magnified and consist principally of influenza-like symptoms, myelosuppression and depression. Newer, pegylated interferon is no better tolerated in HD patients. There are no published series of HBV treatment with interferons in end-stage renal disease (ESRD). There is theoretical concern that they might be less effective given uraemic immune hyporeactivity. Interferons are not recommended in dialysis patients with HBV infection.78

Lamivudine has the longest record of treatment of HBV in dialysis patients, having been introduced in 1998. Lamivudine suppresses viral replication, reduces serum transaminases and improves liver histology in patients with chronic HBV infection and normal renal function.79 Although lamivudine is excreted via the kidneys, dose reduction permits tolerable prescription in patients with impaired renal function.80,81 Good results have been obtained in small case series of HBV-infected patients with renal failure82 with one study of 16 HD patients showing that 56% were able to eliminate HBV DNA and 36% were able to clear HBeAg.83 Unfortunately, HBV resistance to lamivudine develops readily in patients with normal renal function. This has been shown to occur in dialysis patients also, with 10 of 26 (39%) HD or renal transplant patients experiencing viral breakthrough after a median 16.5 months of treatment.84 Despite the risk of mutational resistance, lamivudine needs to be continued for prolonged treatment, as withdrawal has been shown to result in occasional serious relapse episodes in patients with normal renal function, particularly if HBeAg seroconversion has only recently occurred, or not occurred at all.85

Adefovir is a nucleotide reverse transcriptase inhibitor initially developed for use in HIV infection. In an early trial, renal toxicity was evident in 60% of HIV patients treated.86 However, the smaller doses used for HBV infection, and a newer preparation (adefovir dipivoxil) have not shown such severe nephrotoxicity. Provided renal function is monitored carefully, adefovir should be acceptable in patients with impaired renal function.87,88 Adefovir is effective in patients with normal renal function and HBV infection, although a very high relapse rate is seen if adefovir is discontinued: 92% in a study of 185 patients with normal renal function in whom adefovir was withdrawn after 48 weeks of treatment.89 Resistance is much less common than with lamivudine: 0% at one year and 29% at 5 years.90 This makes adefovir an option as add-on therapy in patients who have developed lamivudine resistance.91

Adefovir has not been well examined in patients with renal failure. A French study used adefovir in a composite series of 12 patients with CKD,92 all of whom had lamivudine-resistant HBV. There was a significant fall in HBV DNA levels after a median of 15 months of therapy. Only one of these patients was actually receiving dialysis during the study. A case report described successful treatment of HBV infection in a dialysis-dependent liver transplant recipient who had lamivudine-resistant infection and cirrhosis of the allograft.93

Entecavir is a promising drug in the management of HBV infection. In patients with normal renal function, entecavir has been shown to be superior to lamivudine94 and adefovir95 in reducing HBV DNA levels. Although there are not the long-term data that exist for lamivudine, resistance rates appear to be low. Entecavir has not been studied in dialysis patients, although the dose should be reduced in renal failure.79

Tenofovir, a nucleotide reverse transcriptase inhibitor, is recommended as a first-line oral antiviral in HBV patients with normal renal function.96 Although larger series have not found tenofovir to be culpable in HIV patients with renal failure,97 there have been a number of case reports of tubular toxicity and acute kidney injury98–100 with tenofovir use. This raises concern regarding the potential for nephrotoxicity in dialysis patients with residual renal function. A case report showed that tenofovir was effective in a single HBV-infected HD patient. This paper also assessed tenofovir pharmacokinetics,101 and recommended a dose of 300 mg once a week to prevent accumulation. This was endorsed by the manufacturers in a study of nine HD patients.102

In summary, lamivudine has the most solid body of experience to support its use. Tenofovir and entecavir are likely to be more effective, and tenofovir has been shown to be safe in HD patients, but neither drug has any significant evidence base from this patient group.

Patient selection for drug therapy

Determining which dialysis patients with chronic HBV infection to treat is a matter of controversy. In the case of patients with normal renal function, treatment is recommended for those with active HBV replication (HBeAg positive and/or HBV DNA positive) and raised alanine transaminase (ALT) levels.103 It is clear that patients with ESRD exhibit a different clinical and biochemical picture in chronic HBV infection.104 HD patients with HBV infection are less likely to have a symptomatic acute illness, and are more likely to develop chronic carrier status.105 Serum transaminase levels tend to remain within the normal range, although they have been shown to be significantly higher than in HBV-negative controls in an Italian multicentre study.106 HBV DNA levels too are lower in HD patients than in patients with normal renal function and hepatitis B infection.107 The explanation for these findings is not certain, but it seems that the altered inflammatory response in ESRD and removal of HBV DNA by dialysis are contributory.108 Regardless, the consequence is that selecting those dialysis patients most likely to develop fibrotic liver changes is not possible with conventional assessment of ALT levels and HBV DNA quantification.109

Ideally, treatment of chronic hepatitis B infection would result in HBsAg seroconversion and clearance of HBV DNA. This is uncommon with current therapy. A more pragmatic ambition is to suppress viral replication and thereby prevent, or ameliorate, cirrhosis. It is generally agreed that patients with HBsAg positivity, but undetectable viral replication (from HBeAg and HBV DNA levels) do not warrant antiviral treatment if they are to remain on dialysis, although monitoring for complications such as hepatocellular carcinoma should be undertaken.110 In those who are HBsAg-positive and have evidence of viral replication, liver biopsy should be considered, even in the presence of ‘normal’ ALT levels.19,110 Controversy reigns with regard to subsequent initiation of treatment, but those dialysis patients with high HBV DNA levels, or evidence of active inflammation on biopsy are candidates for antiviral therapy.

With regard to renal transplant candidates, it is recommended that any patient who is HBsAg positive undergo histological liver evaluation.110 Established cirrhosis before transplantation confers an increased risk of mortality and thus is a contraindication to engraftment of a kidney alone.111 Initiation of antiviral therapy before transplantation should be considered where there is evidence of viral replication on blood testing.


Hepatitis B remains a major health issue in dialysis patients. Despite the introduction of effective infection control measures to minimize patient-to-patient transmission, occasional outbreaks occur in dialysis units, usually because of lapses in practice. In many parts of the world hepatitis B is endemic and the high background prevalence of the virus is reflected in the dialysis population. An effective vaccine has made a notable contribution to the protection of dialysis patients from the virus, although this is tempered by reduced potency and durability of the anti-HBs response in those with ESRD. The course of hepatitis B infection is different in patients with dialysis-dependent renal failure. Choosing which patients to treat with antiviral therapy, when, and with which drugs, is a subject of uncertainty at present.