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The patient��s clinical course after the admission is shown in Fig.?1. Despite conservative therapies including blood pressure control, the patient lost her kidney graft and was re-induced into hemodialysis at the 21st gestational week, 49?months after the transplantation. In addition, the patient developed progressive hemolytic anemia, thrombocytopenia, and psychological disorder, including insanity. The patient��s hematological data showed normal coagulability. The activity of a disintegrin-like and metalloprotease with thrombospondin type 1 motifs 13 (ADAMTS13) was significantly low (50.1%), http://www.selleckchem.com/products/epacadostat-incb024360.html and an inhibitor specific to ADAMTS13 was undetected. The kidney allograft biopsy showed endothelial injury and focal eosinophilic materials that seems to be microthrombi in a capillary lumen and tubulitis with interstitial infiltration (Banff t1 and i2). From these findings, the patient was diagnosed as thrombotic microangiopathy concurrent with acute rejection (Fig.?2). The treatment of plasma exchange was initiated immediately as well as MP pulse therapy. Despite eleven sessions of plasma exchange, thrombocytopenia progressed. In addition, the patient developed oligohydramnios and intrauterine growth retardation (IUGR). At the 24th gestational week, the patient underwent a caesarian section. Consequently, the patient recovered from thrombocytopenia drastically without any further treatments. However, the patient lost her neonate five d after giving a birth, and the patient��s graft function had never recovered. TTP is characterized by a moderate to severe thrombocytopenia, red blood cell fragmentation, and an elevated LDH levels. Currently, a pentad of features classically associated with TTP, fever, renal failure, neurologic deficit, and microangiopathic hemolytic anemia is rarely seen (1). TTP sometimes occurs in association with pregnancy, autoimmune disease, allogeneic bone marrow transplantation, infection, and drugs such as calcineurin inhibitor (CNI), mitomycin, and ticlopidine (2). Above all, pregnancy is a prominent risk factor for the development of TTP. TTP is likely to occur during a third trimester or postpartum (3). Another possibility of inducing TTP in our case is the use of CNI. However, in most reported cases of TTP associated with CNI occurred in an early post-transplant period. In our current case, the drastic improvement of thrombocytopenia after the delivery of a baby without any further treatments indicated that pregnancy played a dominant role in inducing TTP. ADAMTS13 is a von Willebrand factor (vWF)-cleaving protease that prevents a formation of unusually large vWF multimer that causes platelet agglutination in the arterial microvasculature (4, 5). Recently, it has been reported that patients with idiopathic TTP have severely decreased activity (