Thrombotic microangiopathy after living-donor liver re-transplantation

Takashi Matsusaki, Hiroshi Morimatsu, Tetsufumi Sato, Kenji Sato, Satoshi Mizobuchi, Kiyoshi Morita

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Thrombotic microangiopathy (TMA) is a rare but potentially lethal complication encountered in solid organ and bone marrow transplant recipients that requires rapid recognition, diagnosis, and initiation of therapy. Several causes have been identified, including viral infections and various medications. We report a case of TMA after living-donor liver transplantation (LDLT). A 60-yearold man underwent LDLT for end-stage liver disease secondary to hepatitis C virus. After 6 months, he required re-transplantation because graft failure was caused by a small-for-size graft. The immunosuppressive regimen for the second transplantation consisted of tacrolimus and prednisolone; cyclosporine (CsA), mycophenolate mofetil, and prednisolone had been used for the first transplantation. Despite multiple transfusions of packed red blood cells and concentrated platelets, his hemoglobin and platelets decreased and lactate dehydrogenase increased following re-transplantation. Hematological evaluation revealed findings consistent with TMA. As soon as TMA was diagnosed, the calcineurin inhibitor (CNI) was changed from tacrolimus to CsA, and fresh frozen plasma (FFP) was given. The patient's platelets gradually increased after the CNI was changed, and no transfusions were needed. Therefore, tacrolimus was suspected as the cause of the patient's TMA. Early diagnosis, switching CNIs, and FFP supplementation allowed the TMA to resolve without the need for plasma exchange.

Original languageEnglish
Pages (from-to)614-617
Number of pages4
JournalJournal of Anesthesia
Issue number4
Publication statusPublished - Aug 1 2010


  • Calcineurin inhibitor
  • Living-donor liver transplantation
  • Thrombotic microangiopathy

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine


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