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Abstract: PO1198

First Report of Simultaneous HBsAg and Anti-HBs Reactivity in a Hemodialysis Patient

Session Information

Category: Trainee Case Report

  • 701 Dialysis: Hemodialysis and Frequent Dialysis


  • Biala, Namita, Lower Bucks Hospital, Bristol, Pennsylvania, United States
  • Sanghi, Pooja, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, United States
  • Goldman, Jesse M., Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, United States

Of great concern to dialysis units is the presence of bloodborne pathogens. The incidence of HBV infection is quite low in the United States, however outbreaks of hepatitis B in hemodialysis units have occurred. CDC guidelines recommend hemodialysis patients be screened for HBV surface antigen (HBsAg) surface antibody (anti-HBs) and core antibody (anti-HBc) on admission to the dialysis unit. We present an usual case of a patient with both HBsAg and anti-HBs positive who required hemodialysis (HD).

Case Description

A 78-year-old Chinese female with past medical history of CKD stage V, Type 2 DM, hypertension, chronic HBV with no prior treatment, presented to the ED with signs of fluid overload. In the ED she was hypertensive to 170/107. Labs showed a creatinine of 5.7 (baseline) and a serum sodium of 116. Liver enzymes were mildly elevated with no associated jaundice. Physical exam showed +2 peripheral edema and bilateral crackles, neither abdominal tenderness nor scleral icterus was present. No neurological deficits appreciated. Acute coronary syndrome was excluded. She was admitted and scheduled for hemodialysis. Admission labs showed anti-HBc positive, HBsAg positive, as well as anti-HBs positivity. Confirmatory HBV quantitative PCR testing resulted at 28 IU/ml.


Classically, anti-HBs antibodies neutralize and clear HBsAg from peripheral blood. Therefore, the presence of anti-HBs is considered an indicator of immunity from ongoing HBV infection. The typical serological feature of chronic HBV infection is circulating HBsAg and lack of anti-HBs. However, the coexistence of HBsAg and anti-HBs has been reported to be as high as 8% of chronic HBV patients. The coexistence of HBsAg and anti-HBs has been explained by the phenomenon of “escape variation”. Point mutations or deletions in the pre-S/ S gene of HBsAg may give rise to mutant surface proteins. The detectable HBsAg is thus a mixture of wild type and variants, whereas the detectable anti-HBs are only against wild type viruses. These patients are still in the chronic HBV infection category as they typically do not progress to active disease, however acute infection is possible. Given our patient’s low HBV DNA (< 10,000 IU/ ml) and mild transaminitis, she fits the chronic, inactive carrier state. Appropriate infection control precautions for HD were taken as established for chronic HBV infection patients.