Von Willebrand factor-cleaving protease activity in thrombotic microangiopathy after living donor liver transplantation: A case report

Nakazawa, Yūichi; Urata, Koichi; Ikegami, Toshihiko; Terada, Masaru; Yano, Hideo; Ishizashi, Hiromichi; Matsumoto, Masanori; Fujimura, Yoshihiro; Miyagawa, Shinichi

doi:10.1016/j.lts.2003.09.021

Cited by 34 publications

(25 citation statements)

References 20 publications

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“…It is interesting that several groups have suggested that varying assays of ADAMTS13 activity and inhibitors are useful to predict clinical outcomes of patients who have TMA and are treated with plasma therapy (46,47). Nevertheless, it remains controversial whether a similar mechanism or clinical approach can be valid with patients who develop TMA after solid-organ transplantation, according to case reports that have evaluated this enzyme activity in blood samples of these patients (48,49). Unfavorable responses to PE in this report might be explained by different pathophysiology from deficiency in those factors, but these molecules were not examined in our study.…”

Section: Prognostic Analysesmentioning

confidence: 99%

Clinical Outcome of Thrombotic Microangiopathy after Living-Donor Liver Transplantation Treated with Plasma Exchange Therapy

Nishi

Hanafusa²,

Kondo³

et al. 2006

Clinical Journal of the American Society of Nephrology

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Section: Prognostic Analysesmentioning

confidence: 99%

Clinical Outcome of Thrombotic Microangiopathy after Living-Donor Liver Transplantation Treated with Plasma Exchange Therapy

Nishi

Hanafusa²,

Kondo³

et al. 2006

Clinical Journal of the American Society of Nephrology

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“…10 This factor has been proposed to play a major role in the pathogenesis of TMA. Nakazawa et al 15 hypothesized that the severity of the vWF-cleaving protease deficit might be involved in the occurrence of TMA in LDLT recipients because vWF-cleaving protease is exclusively synthesized in the liver and the small-for-size graft in LDLT might have a reduced capacity to produce the enzyme. However, the vWF-cleaving protease level is higher in healthy individuals of blood group O than those of non-O blood groups.…”

Section: Discussionmentioning

confidence: 99%

“…12,13 However, TMA also can occur in living donor liver transplantation (LDLT) and, to date, there have been sporadic reports of TMA in LDLT recipients. 11,14,15 A total of 106 patients underwent LDLT for various terminal liver diseases at Keio University Hospital (Tokyo, Japan). Of the 106 patients, 4 (3.7%) presented with TMA after LDLT in our institution.…”

mentioning

confidence: 99%

Clinical characteristics of thrombotic microangiopathy following ABO incompatible living donor liver transplantation

et al. 2007

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Thrombotic microangiopathy (TMA) may develop after living donor liver transplantation (LDLT), but the mechanism is not fully understood. We retrospectively analyzed all patients undergoing LDLT at our center, including TMA patients, to elucidate the clinical characteristics and presentation and to determine which patients have a higher risk of occurrence of TMA. In all, 57 adult patients were reviewed after LDLT at our institution. TMA was diagnosed by sudden and severe thrombocytopenia, followed by hemolytic anemia with fractionated erythrocytes in the blood smear. Clinical features were compared between the TMA group and the non-TMA group. Of the 57 patients, 4 were diagnosed with posttransplantation TMA. ABO blood group (ABO)-incompatibility, cyclophosphamide (CPA), and recipient blood group (type O) were closely correlated with the occurrence of TMA. Thrombocytopenia appeared 1 to 5 days before hemolytic anemia. Coagulative function markers stayed at the same level after TMA, while marked elevation was shown in fibrinolytic function markers such as plasminogen activator inhibitor type 1 (PAI-1). TMA occurred at a higher prevalence in ABO-incompatible graft recipients. Additional factors associated with ABO-incompatible transplantation, such as an overdose of immunosuppressants, may affect the likelihood of TMA. Sudden and severe thrombocytopenia presented before hemolytic anemia and the serum levels of PAI-1 correlated well with the clinical course of TMA. In conclusion, early recognition of thrombocytopenia and elevation of PAI-1 is crucial to diagnose TMA especially in ABO-incompatible LDLT.

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“…29 However, there are reported cases of severe deficiency of ADAMTS-13 activity in lung transplant patients presenting with diffuse alveolar haemorrhage. 30 In our series, ADAMTS-13 activity level was normal in two patients tested.…”

mentioning

confidence: 99%

“…Interpretation of ADAMTS 13 activity following liver transplant may be difficult as it is produced primarily in the liver, and levels may be low in the immediate posttransplant period due to graft ischaemia-reperfusion injury. 29 As such, monitoring of ADAMTS 13 activity should be considered on a case-by-case basis. 31 Serum tacrolimus levels were measured in two cases of tacrolimus-associated TMA following renal transplantation, and no correlation was found between the trough level of tacrolimus and the development of TMA.…”

mentioning

confidence: 99%

Tacrolimus‐induced thrombotic microangiopathy in orthotopic liver transplant patients: case series of four patients

Nwaba¹,

MacQuillan²,

Adams³

et al. 2013

Internal Medicine Journal

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Thrombotic microangiopathy (TMA) is a potentially fatal complication in solid organ and bone marrow transplant patients, with reported incidence of 0.5-3% and mortality of about 75%. To emphasise the importance of early diagnosis and prompt commencement of therapy results in improved clinical outcomes. A retrospective study of all patients who underwent orthotopic liver transplantation (OLTX) at the Western Australian Liver Transplantation Service from May 1994 to December 2010 was conducted to identify patients who developed tacrolimus-induced TMA. We identified four patients with tacrolimus-induced TMA post-OLTX, derived from a cohort of 104 patients treated with tacrolimus in our institution. The mean age at diagnosis was 40 years, and the mean time of onset was 63 Ϯ 7.5 weeks after OLTX. The indications for OLTX in the four patients were fulminant hepatic failure in three (Wilson disease, paracetamol overdose and post-partum thrombotic thrombocytopenic purpura) and hepatitis C virus-related cirrhosis. All patients had tacrolimus post-OLTX. At diagnosis, tacrolimus was discontinued in all patients, and three of the four patients underwent plasma exchange and all patients improved clinically. Mean duration of follow up was 15 Ϯ 7.5 months. There was no mortality 6 months post-TMA. Early diagnosis with immediate discontinuation or conversion of calcineurin inhibitors and plasma exchange should be offered to OLTX patients with TMA as it results in good outcomes.

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Von Willebrand factor-cleaving protease activity in thrombotic microangiopathy after living donor liver transplantation: A case report

Cited by 34 publications

References 20 publications

Clinical Outcome of Thrombotic Microangiopathy after Living-Donor Liver Transplantation Treated with Plasma Exchange Therapy

Clinical Outcome of Thrombotic Microangiopathy after Living-Donor Liver Transplantation Treated with Plasma Exchange Therapy

Clinical characteristics of thrombotic microangiopathy following ABO incompatible living donor liver transplantation

Tacrolimus‐induced thrombotic microangiopathy in orthotopic liver transplant patients: case series of four patients

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