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Hepatitis B infection in Chronic Kidneydisease
Hepatitis B virus (HBV) infection poses unique challenges for patients with chronic kidney disease (CKD), particularly those on dialysis, due to their immunocompromised state and the risk of asymptomatic infections. Prevention strategies, including vaccination and universal precautions, are critical to reducing HBV transmission in dialysis units, while management may involve antiviral therapies tailored to the patient's renal condition. In renal transplant recipients, thorough screening and preventive measures are essential to mitigate the risk of HBV reactivation, with comparative strategies for managing preemptive or prophylactic antiviral treatments being recommended.
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Hepatitis B infection in CKD is a clinical issue due to immune suppression and affects morbidity and mortality.
Natural history of HBV varies; endemic areas have childhood infections while non-endemic areas are adult-acquired.
Dialysis patients are prone to chronic HBV with mild symptoms; infection rates reflect endemicity. Peritoneal dialysis carries lower risk.
HBsAg is diagnostic for HBV. PCR offers higher sensitivity for occult infections.
Universal precautions, vaccination, and infection control are essential in preventing HBV transmission in dialysis units.
Vaccination efficacy is moderate in ESRD. Enhanced doses and protocols are suggested to improve response.
Regular monitoring and treatment are crucial in managing HBV infection and preventing complications in CKD patients.
HBV management is critical before and after renal transplant. Strategies include prophylactic therapies to prevent reactivation.
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Hepatitis B infection in Chronic Kidneydisease
- 1. HEPATITIS B INFECTIONIN CKD PATIENTS Dr AJISH JOHN
- 2. Introduction HBV infectionin CKD patients presents a distinct clinical problem. immunosuppressive effect of renal failure Susceptibility for de novo infection and nosocomial transmission long-term implications on morbidity and mortality change in clinical course after kidney transplantation.
- 3. Natural history varyaccording to the timing of infection, genotype, and locality. Endemic areas – mostly carriers who acquired infection during childhood Non-endemic areas – acquired during adulthood.
- 4. HEMODIALYSIS & CAPDIN HEPATITIS B INFECTION
- 5. Peculiarities of HBVin dialysis patients more prone to become chronic carriers due to their immunosuppressed state. Relatively mild clinical course. Infection often asymptomatic Normal or only slight elevation of transaminase.
- 6. Incidence & Prevalence Factors causing decreasing prevelance of HBV infection in dialysis patients – Screening of blood products for HBsAg and anti-HBc Implementation of infection control measures Reduced need for transfusion after the advent of erythropoietin Hepatitis B vaccination
- 7. HBsAg positivity ratesin dialysis patients correlate with endemicity in the general population. 1% in United States 5.9% in Italy 12% in Brazil 1.3-14.6% in Asian Pacific countries
- 8. RISK FACTORS FORHBV INFECTION IN DIALYSIS UNITS Presence of HBsAg positive patients within the same dialysis unit Nonsegregation with dedicated hemodialysis machines for HBsAg positive patients Lower prevalence rate of hepatitis B vaccination among dialysis patients in the same unit
- 9. Even in HBsAg-negativedialysis patients with a history of resolved HBV infection, minute amounts of transcriptionally active HBV DNA could be detected by PCR This phenomenon is associated with deletions in the pre-S1 region of the viral genome, which affected the S promoter, thereby reducing the production of HBsAg.
- 10. Although HBV DNAtraverses the dialyzer membrane during high flux dialysis, the degree of infectivity of dialysate and ultrafiltrate remains controversial. Patients on peritoneal dialysis have a lower risk of acquiring HBV infection compared to those on long-term hemodialysis.
- 11. DIAGNOSIS OF HBVINFECTION HBsAg is sufficient for the diagnosis of HBV infection Quantitative real-time PCR assays for HBV DNA offer increased sensitivity with detection threshold down to 20 IU or 102 copies/mL. Occult HBV infection – neg HBsAg
- 12. Occult HBV infection– positivity in nested PCR assays for the pre-S/S, pre- Core/Core, and X viral regions with sensitivity down to 10 copies/mL.
- 13. Recommended HBV testingin MHD
- 14. PREVENTION MEASURES Universalprecautionary measures Hemodialysis unit procedures for the prevention of blood borne infections Hepatitis B vaccination
- 15. Barrier procedures toprevent exposure to blood borne microorganisms :- Washing hands after contact with potentially infectious surface or material Wearing gloves when contacting potentially infectious surface or material Wearing a face mask and gown when exposure to blood or body fluids is expected
- 16. Segregation and reuseof dialyzers Machine segregation & separate HD room is now standard practice. Dialyzer reuse was also not associated with a higher risk of HBV infection both in patients and in staff. CDC recommendation - dialyzers from HBsAg-positive patients be excluded from reuse programs
- 17. Hepatitis B vaccination Risk of HBV infection reduced by 70% with vaccination. CDC recommend routine vaccination in all dialysis patients.
- 18. Arguments against vaccination– Reduced efficacy of vaccine in ESRD – Seroconversion – only 50-60% Immune response correlate with degree of renal failure Low rate of HBV infection (0.12% among HD pts)
- 19. Vaccination failure – Anti HBsAg titer ≤ 10 IU/L (1-2 months after completion of vaccination schedule)
- 20. Measures to enhanceimmune response – Double vaccine dose (40mcg/dose) Administer in deltoid Additional doses (0,1,2,6 months) Administer early before GFR declines
- 21. Administer additional threedose series to dialysis patients with vaccination failure Administer single booster dose of 40mcg if antibody titer fall to ≤ 10 IU/L after initial response. Intradermal vs intramuscular Role of adjuvants
- 22. An accelerated scheduleof 0, 7, 21 days and 12 months may be used. Post vaccination serological testing - 3 months after the third dose of hepatitis B vaccine. Anti-HBs levels >10mIU/ml are considered to be protective.
- 23. Due to chanceof spurious seropositivity for HBsAg, testing of serum for HBsAg should be avoided within 3 weeks of vaccination. No role for repeated boosters in those whose antibody titers remain ≤ 10 IU/L. Despite vaccination the most important factor in preventing spread of HBV is - Maintenance of universal precautions.
- 24. CAPD in HepatitisB patients Preferred modality of RRT in HBV infected CKD patients. Avoids risk to health personnel Economic, avoids segregation, no risk to other patients Easy to dispose PD fluid effluent Minimal risk to household members.
- 25. CAPD in Cirrhoticpatients – No increased risk of CAPD peritonitis Avoids risk of heparinisation Provides added calorie Increased protein loss
- 26. Method of disinfectionof CAPD bags & effluent - A cupful of household bleach should be poured into the toilet and the bag drained into this. The toilet should be flushed after 5 min. The emptied CAPD bags should be placed in a plastic bag to which a small quantity of bleach has been added.
- 27. CLINICAL MANIFESTATIONS Upperlimit of transaminases in dialysis pts – SGOT < 24 IU/L SGPT < 17 IU/L
- 28. Acute infection Extremelyvariable manifestations Majority – Asymptomatic Mild symptoms Only mild elevation of transaminases
- 29. Serotype may affectseverity Precore mutants have severe presentation Majority become chronic carriers (80%)
- 30. Chronic infection Manifestationof chronic infection or cirrhosis in dialysis pts identical to those without renal failure. Aminotransferase level should to interpreted accordingly. Screen for Hepatitis D virus coinfection. Histological evidence of chronic hepatitis in 30% of dialysis pts with HBV infection.
- 31. Prior to availabilityof nucleoside analogues clinical outcome in dialysis patients were inferior. Only less than 5% of dialysis pts with chronic HBV die of liver disease. Majority of death is due to CVDs.
- 32. Cirrhosis associated with35% increase in mortality rate among dialysis pts. Whether HBV infection has adverse effect on patient survival is controversial.
- 33. MANAGEMENT OF HBVIN CKD
- 34. Periodic monitering - ALT/AST, Albumin every six to eight week intervals. USG abdomen to assess liver & αFP annually.
- 35. Elastography to assessliver stiffness – role not established. Role of Liver Biopsy – Best assess activity, extent of cirrhotic changes Recommended prior to antiviral treatment Preferred prior to renal transplantation
- 36. Decision to treatHBV – Abnormal AST & ALT HBV DNA > 105 copies/ml or 20,000 IU/ml ( if HBeAg +ve) > 104 copies/ml or 2,000 IU/ml (if HBeAg –ve) Based on liver biopsy – if cirrhosis or not
- 37. Based on – AASLD Guideline (2009) EASL Guideline (2009)
- 38.
- 40. Interferon α –10 MU s/c thrice weekly Pegylated Interferon α Peg IFN α 2a – 180μg s/c weekly Peg IFN α 2b – 1 μg/kg s/c weekly Nucleoside/nucleotide analogues Lamivudine – 100mg/d Adefovir – 10mg/d Tenofovir – 300mg/d Entecavir – 0.5mg/d Telbivudine – 600mg/d
- 41. Duration of treatment Drug HBeAg +ve HBeAg -ve Interferon α 16 wks 1 yr Lamivudine 1 yr > 1yr
- 45. Interferon α Littledata among dialysis patients. 3 MU thrice weekly Due to decreased clearance in ESRD pts – longer t1/2 Side effects are more pronounced in dialysis pts. Exacerbation of anemia and protein malnutrition.
- 46. Pegylated IFN Efficacyand safety of pegylated interferon in ESRD and dialysis patients not defined. HD has only negligible effects on clearance of pegylated IFN. Pegylated IFN not tolerated by majority of HD pts in small trials. is best avoided in HD pts.
- 47. Nucleoside/nucleotide analogues Lamivudine Useful in dialysis pts & post Tx Normalise AST&ALT - >80% HBeAg clearance – 20% Suppress HBV DNA to undetectable level – 50-90%
- 48. Selection of drugresistant variants - YMDD 15% of pts after 12 months of Rx. No longer regarded as preferred first line therapy. Dose in ESRD – 25mg/day
- 49. Entecavir Recommended firstline oral therapy in pts with renal disease. Dose in ESRD on dialysis – 0.05mg/d or 0.5mg/wk 0.1mg/d or 1mg/wk (lamivudine resistant HBV)
- 50. Adefovir & Tenofovir– Nephrotoxic Lead to renal tubular dysfunction Preferably avoided in dialysis pts with residual renal function.
- 51. Rx in Lamivudineresistant HBV – Adefovir add on therapy Tenofovir – more effective than adefovir Entecavir – recommended therapy in ESRD pts Preferably avoid adefovir & tenofovir due to their nephrotoxic potential.
- 52. Start effective treatmentearly after emergence of lamivudine resistance. Helps to prevent hepatitic flares Reduce risk of subsequent development of multiple drug resistance.
- 53. HBV infection inRenal transplant recipients
- 54. Prevelance in endemicareas – 15% Declining trend due to HBV vaccination All patients undergoing renal transplantation should be tested for HBV DNA & HBeAg prior to Tx.
- 55. HBsAg positivity isassociated with increased risk of death and allograft loss. Liver disease is a leading cause of death among renal transplant recipients with c/c HBV. With advent of antiviral therapy overall prognosis has improved.
- 56. HBV infection withESRD can be recommended for Renal Tx only if they do not have cirrhosis. If Cirrhosis present – Combined liver & kidney Tx required.
- 57. All HBsAg +vecandidates for solid-organ Tx should be treated with NAs before Tx. to maintain undetectable HBV DNA, reduce liver fibrosis & prevent hepatic decompensation after Tx. ( EASL clinical practice Guidelines )
- 58. Risk factors forreactivation Due to immunosuppressive therapy Status of recipient – serologic & virologic markers Serologic & virologic status of donor – risk factor for de novo HBV infection.
- 59. Donor Recepient Risk HBsAg +ve HBsAg –ve +++ HBsAg –ve Anti HBc +ve HBsAg –ve ++ HBsAg +ve Anti HBc +ve +
- 60. Increase in HBVDNA precede transaminitis. Result in hepatitis flares Decreased allograft & patient survival Risk of hepatic failure & death
- 61. Preventive therapy Recommendedfor all patients with HBV infection undergoing renal Tx. 2 approaches to prevent post Tx HBV reactivation – 1. Prophylactic strategy 2. Preemptive strategy
- 62. Preemptive strategy Periodicmonitoring for viremia after Tx Prompt Rx after detection or marked rise of HBV DNA in PCR. Require close monitoring which may not always be clinically feasible.
- 63. Prophylactic strategy Administrationof antiviral agents to patients at increased risk of reactivation. Given either prior to or immediately after Tx. Whom to give ? Those pior to TX – +ve HBeAg detectable HBV DNA
- 64. Duration of antiviralprophylaxis – No definite consensus Atleast first 2 years (KDIGO) continue for as long as immunosuppressive therapy lasts. (Shibolet et al)
- 65. Either preemptive orprophylactic strategy provides superior outcomes compared with treatment only after clinically significant reactivation of HBV. Hence preventive therapy is recommended to renal Tx recepients infected with HBV.
- 66. Rx after hepaticdysfunction or transaminitis is detected - less effective in preventing hepatic flares or decompensation than either preventive strategy.
- 67. Antiviral agent – Entecavir – agent of choice Lamivudine Interferon therapy is contraindicated due to risk of acute rejection and low antiviral potency.
- 68. Effective NA therapyincreased patient (81–89%) and graft survival (86%) at 10 years. Due to inhibition of viral replication, retardation of liver disease progression & lower incidence of hepatocellular carcinoma.
- 69. Pts with detectableHBV DNA prior to Tx PROPHYLACTIC THERAPY Prior to or at time of Tx. Preferred agent - ENTECAVIR
- 70. Pts infected withHBV but without detectable HBV DNA prior to Tx PREEMPTIVE STRATEGY Moniter HBV DNA every 3 months for 1st year and then every 6 months Entecavir is initiated when HBV DNA become detectable or increase progressively.
- 71. Pts with antiHBcAg +ve but HBsAg neg PREEMPTIVE STRATEGY Monitor ALT if transaminitis Check HBV DNA
- 72. All patients withe/o HBV infection pre Tx should be closely monitered for viral relapse, hepatitis flare. Liver biopsy can guide decision regarding antiviral treatment in post Tx patients.
- 73. HBV-positive renal transplantdonors Kidneys from HBsAg +ve, but even from HBsAg-neg, anti-HBc +ve donors are not promoted. Due to potential to transmit HBV to recipient
- 74. HBsAg-negative recipients receivinggrafts from anti- HBc +ve donors – Lamivudine prophylaxis Anti-HBsAg +ve recipients receiving grafts from HBsAg +ve donors – Lamivudine combined with immunoglobulin