Second, whether the initial diagnosis of AA should have been hypocellular MDS is uncertain. creatinine (from 2.86?mg/dL to 5.58?mg/dL) and ST7612AA1 uric acid levels (from 10.2?mg/dL to 32.7?mg/dL), which suggested acute uric acid nephropathy. Tumor lysis syndrome was suspected to be the cause ST7612AA1 of the acute uric acid nephropathy; hence, the patient was reevaluated for aplastic anemia. Human leukocyte antigen-DR15 was positive, and flow cytometry revealed a low percentage of glycophosphatidyl inositol-deficient granulocytes (2.9%), which suggested paroxysmal nocturnal hemoglobinuria clones. These findings indicate that this previously diagnosed aplastic anemia had either originally been hypocellular myelodysplastic syndrome (MDS) or later transformed into hypocellular MDS, which is a type of bone marrow failure syndrome. Conclusions Clinicians should consider unexpected tumor lysis syndrome to be the cause of complications after antithymocyte globulin treatment in kidney transplant recipients with underlying bone marrow failure syndrome. Hemoglobin; Platelet; Blood urea nitrogen; Creatinine; Lactate dehydrogenase; Creatine phosphokinase; High power field Two hemodialysis sessions were completed because of oliguria (urine output, ?200?mL/day). After hemodialysis, the patients serum uric acid and Cr levels remained at 3.3 and 3.96?mg/dL, respectively, with a daily urine output of ?1500?mL, and she was discharged (Fig. ?(Fig.2).2). TLS was suspected to be the cause of the acute uric acid nephropathy; therefore, post-transplantation lymphoproliferative disorder was considered a possibility. Epstein-Barr virus was not detected, and the imaging studies showed no findings indicative of lymphoma. Thus, the patient was reevaluated for the underlying hematologic disease. Flow cytometry of the paroxysmal nocturnal hemoglobinuria (PNH) clones revealed a 2.9% glycophosphatidyl inositol (GPI)-deficient granulocyte and a 2.9% CD24-deficient granulocyte expansion, which suggest that either the AA transformed into myelodysplastic syndrome (MDS) or the original underlying disease was MDS. Unfortunately, the patient progressed to graft failure 2?months after discharge and resumed PD. Discussion and conclusions The present case demonstrates the occurrence of an extremely high increase in serum uric acid level ( ?30?mg/dL) and AKI after ATG treatment in a KT recipient with underlying AA. We diagnosed the case as TLS based on the criteria for hyperuricemia, hyperphosphatemia, hyperkalemia, and AKI [9]. TLS usually presents within 7?days of cytotoxic ST7612AA1 chemotherapy [5] and most often occurs in hematologic malignancies with high turnover rates, such as AML and ALL, but is rarely reported in bone marrow failure syndromes such as AA and MDS [7, 9]. This is the first report of acute uric acid nephropathy presumably caused by ATG treatment-related TLS in a KT recipient with a previous diagnosis of AA. TLS development after ATG treatment is usually unusual. This case was characterized by a long, 8-year history of AA with gradual improvement after kidney transplantation. Thus, the underlying AA was considered the cause of the TLS. A case review revealed two interesting findings. First, the patient was HLA-DR15 positive. In previous studies, AA patients with HLA-DR15 positivity showed 8.53 times higher hematologic improvement with immunosuppressants and higher coexisting PNH and MDS rates than the negative group [10, 11]. Second, the patient had PNH clones (2.9% GPI- and 2.9% CD24-deficient granulocytes), which suggested subclinical PNH. These features were consistent with those of a previous report that subclinical PNH in MDS patients showed a high HLA-DR15 positivity rate (90.5%) and bone marrow hypocellularity ST7612AA1 (64.3%). In addition, these patients often have normal karyotypic morphologies (95.2%) and respond well to immunosuppressants (77.8%) [12], as observed in the bone marrow biopsy findings from our case (Fig. ?(Fig.1).1). All the findings showed the possibility that the patient in this report either originally had hypocellular MDS or a previously diagnosed AA that had transformed into another type of bone marrow failure syndrome owing to clonal evolution [13, 14]. One may argue that high-dose methylprednisolone rather than ATG is responsible for the TLS in ST7612AA1 this case. Indeed, the Rabbit polyclonal to AGO2 development of TLS after high-dose methylprednisolone administration in MDS was previously reported [7]. In the review of our case, the patient was administered high-dose methylprednisolone two times with a 1-month interval (acute rejection treatment and premedication for ATG). If the high-dose methylprednisolone administration was responsible for the TLS in our case, TLS should have occurred during the first administration of methylprednisolone for acute rejection treatment. Thus, we suggest ATG, rather than methylprednisolone, to be the cause of the TLS, and that the possible pathophysiology of the ATG therapy-related TLS in MDS is the presence of potentially chemosensitive hematologic malignant cells. This presumption may be supported by a previous report of rapid tumor cell lysis occurring after ATG therapy for Sezary syndrome (cutaneous T-cell lymphoma) [15]. In this case, mizoribine was used as a maintenance immunosuppressant. Previous studies reported that mizoribine might cause hyperuricemia in patients with renal dysfunction [16, 17]. Mizoribine use may have contributed to the extreme hyperuricemia in this case; however, despite.