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Published on: December 15, 2011
Cryoglobulinemia presenting after liver transplantation
J Gournay1, L D Ferrell, J P Roberts
1Department of Medicine, University of California, San Francisco, USA.
Insights
Essential mixed cryoglobulinemia, often linked to hepatitis C, can manifest post-liver transplant. This study highlights three cases where cryoglobulinemia with vasculitis emerged after transplantation, emphasizing the role of hepatitis C virus (HCV) infection.
Area of Science:
- Nephrology
- Hepatology
- Immunology
Background:
- Essential mixed cryoglobulinemia is commonly associated with chronic hepatitis C infection.
- Hepatitis C virus (HCV) is a significant etiologic factor in the development of cryoglobulinemia.
Observation:
- This report details three patients who developed cryoglobulinemia with vasculitis after undergoing liver transplantation for end-stage chronic hepatitis C.
- HCV infection was confirmed via HCV RNA detection. Vasculitis symptoms appeared 1, 5, and 17 months post-transplantation.
- Patients presented with Type II cryoglobulins, cutaneous vasculitis, and in two cases, membranoproliferative glomerulonephritis.
Findings:
- Post-transplant cryoglobulinemia can present with severe manifestations including cutaneous vasculitis and glomerulonephritis.
- Treatment responses varied; one patient improved with plasmapheresis and cyclophosphamide, while another experienced irreversible renal failure.
- Complications included digital amputation, autoimmune hemolytic anemia, and multiorgan failure, leading to one fatality.
Implications:
- HCV-associated cryoglobulinemia may become clinically significant after liver transplantation, potentially due to increased post-transplant viremia.
- These findings underscore the importance of monitoring for cryoglobulinemia in HCV-infected patients post-transplantation.
- Further research is warranted to understand the mechanisms driving post-transplant cryoglobulinemia and to optimize management strategies.
Abstract:
Essential mixed cryoglobulinemia is frequently associated with chronic hepatitis C. Three patients undergoing transplantation for end-stage chronic hepatitis C in whom cryoglobulinemia with vasculitis developed after transplantation are described. Hepatitis C virus (HCV) infection was confirmed in the 3 patients by the presence of HCV RNA detected by polymerase chain reaction. The time interval between transplantation and the first expression of vasculitis was 1, 5, and 17 months. Type II cryoglobulins were detected in the sera of all 3 patients. All patients developed cutaneous vasculitis, requiring digital amputation in 1 case. Two patients developed membranoproliferative glomerulonephritis. Plasmapheresis and the addition of cyclophosphamide led to an improvement in the renal disease in 1 case, whereas no treatment was able to reverse the renal failure in the other case. One patient developed an autoimmune hemolytic anemia 4 years after transplantation. One patient died of multiorgan failure 5 months after transplantation. We propose that HCV-associated cryoglobulinemia could become clinically significant only after orthotopic liver transplantation, possibly due in part to posttransplant increase in viremia as reflected by HCV RNA levels. These results confirm previous observations suggesting that HCV infection is important etiologically in the pathogenesis of cryoglobulinemia.
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