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Thrombotic microangiopathy in living-donor liver transplantation
Sumihito Tamura1, Yasuhiko Sugawara, Yuichi Matsui
1Artificial Organ and Transplantation Division, Department of Surgery, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Background:
Thrombotic microangiopathy (TMA) is a fatal complication characterized by microvascular occlusive disorder resulting in systemic or intrarenal platelet aggregation, severe thrombocytopenia, and microangiopathic hemolytic anemia. Only sporadic case reports of TMA after cadaveric or living-donor liver transplantation (LDLT) have been described.
Methods:
The authors report 10 (5% of the total series) TMA patients after LDLT and review the previously reported cases. TMA was diagnosed on the basis of progressive thrombocytopenia of unknown cause and microangiopathic hemolytic anemia, suggested by sharp elevation of serum lactate dehydrogenase levels and the presence of fractionated erythrocytes in blood smear.
Results:
Of the 10 patients with TMA, 7 presented with viral hepatitis (2 with hepatitis B and 5 with hepatitis C virus infection) as the cause of end-stage liver disease. Clinical diagnosis of TMA was made at a median interval of 18 days (range, 3-356 days) from the time of transplantation. Conversion of calcineurin inhibitors (CNI) was conducted in nine patients. One patient recovered after CNI conversion alone. Plasma exchange was performed in eight patients. Three patients died.
Conclusions:
Immediate treatment of TMA should be initiated by reduction or conversion of CNI followed by plasma exchange. Hepatitis C virus infection might contribute to the high incidence of TMA in LDLT patients.
Insights
Thrombotic microangiopathy (TMA) is a rare but serious complication after liver transplantation. Early treatment involving calcineurin inhibitor adjustment and plasma exchange improves outcomes for these patients.
Area of Science:
- Nephrology
- Hepatology
- Transplantation Medicine
Background:
- Thrombotic microangiopathy (TMA) is a severe complication characterized by platelet aggregation, thrombocytopenia, and hemolytic anemia.
- TMA following liver transplantation, particularly living-donor liver transplantation (LDLT), is infrequently reported.
Purpose of the Study:
- To report the incidence and characteristics of TMA in LDLT recipients.
- To review previously reported cases and analyze treatment outcomes.
Main Methods:
- Retrospective analysis of 10 TMA cases post-LDLT.
- Diagnosis based on thrombocytopenia, microangiopathic hemolytic anemia, elevated LDH, and schistocytes.
- Review of existing literature on TMA post-liver transplantation.
Main Results:
- TMA occurred in 5% of LDLT patients, with a median diagnosis interval of 18 days post-transplant.
- Hepatitis C virus infection was present in 5 of 10 patients with end-stage liver disease.
- Seven of 10 patients received calcineurin inhibitor (CNI) conversion; one recovered with CNI conversion alone. Eight patients underwent plasma exchange, and three died.
Conclusions:
- Prompt management of TMA post-LDLT involves CNI modification and plasma exchange.
- Hepatitis C virus infection may be a contributing factor to TMA development in LDLT recipients.
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