Many of the complications experienced by patients undergoing hemodialysis can be attributed to their altered host defenses. Increased cutaneous staphylococcal carriage along with repeated intravascular cannulation and defective mucocutaneous barriers lead to frequent invasion by infectious agents. Pathogens encounter granulocytes with subnormal locomotion, phagocytosis, and intracellular killing. Depressed cell-mediated immunity may be explained by shortened lymphocyte survival, lymphopenia, inhibition of lymphocyte transformation, and suppressor T-cell activity. This is manifested by cutaneous anergy, prolonged graft survival, altered tumor surveillance, and abnormal responses to hepatitis B and tuberculosis. Host interaction with the hemodialysis membrane leads to cellular disruption, which may induce autoantibodies. Activation of the alternate complement pathway during hemodialysis leads to granulocyte sequestration in small vessels, specifically within the lungs. These hemodialysis-induced alterations along with the manifestations of underlying chronic renal insufficiency may obscure clinical evaluation of these patients.

Host Defenses and Immunologic Alterations Associated with Chronic Hemodialysis

https://www.gastrojournal.org/article/S0016-5085(81)80002-9/pdf

Effects of Immunosuppressive Therapy on Viral Markers in Chronic Active Hepatitis B

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.1840030309

Natural History of Hepatitis B Virus Infection in Renal Transplant Recipients–A Fifteen-Year Follow-Up

— We studied liver biopsies performed between January 1972 and June 1980 in 111 patients receiving regular dialysis treatment. Biopsies were performed either because of suspected liver disease (61 patients) or routinely during abdominal surgery or kidney transplantation (50 patients). Repeat biopsies were done in 14 cases. Hepatitis B virus markers, assayed every 3 months during the observation period, were detected at some time in 71 patients (64%); 51 remained persistently positive. Histological examination showed normal liver in 39 cases, lobular hepatitis in 15, chronic persistent hepatitis in 36 and chronic active hepatitis in 21. All patients with chronic active hepatitis were chronic HBsAg carriers, and repeated biopsies showed aggravation only in these patients. The course was remarkably asymptomatic, with lesions leading to fibrosis despite the lack of histopathological patterns of severe necrosis and/or inflammation, which were conspicuously absent in this series.

Relationship between liver histopathological changes and HBs Ag in 111 patients treated by long‐term hemodialysis

Keywords:

anti-HBe;
HBeAg;
HBV DNA;
chronic HBV infection;
chronic type B hepatitis;
cirrhosis;
HBsAg carriers;
hepatocellular carcinoma.

James Grant

Papers

Hepatitis B in hemodialysis patients: Significance of HBeAg