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Acute kidney injury with extreme hyperuricemia after antithymocyte globulin treatment in a kidney transplant recipient with underlying aplastic anemia: a case report.
BMC Nephrology ( IF 2.2 ) Pub Date : 2020-07-02 , DOI: 10.1186/s12882-020-01903-9
Yohan Park 1 , Byung Ha Chung 1 , Cheol Whee Park 1 , Yong-Soo Kim 1 , Chul Woo Yang 1
Affiliation  

The occurrences of hyperuricemia and acute kidney injury after antithymocyte globulin treatment are unusual in kidney transplant recipients. Here, we report a unique case of acute kidney injury with extreme hyperuricemia after antithymocyte globulin treatment in a kidney transplant recipient with underlying aplastic anemia. A 40-year-old woman with aplastic anemia who received a kidney transplant 5 years 6 months before presented to our emergency department with complaints of oliguria, generalized edema, and general weakness 6 days after receiving antithymocyte globulin treatment for acute T-cell-mediated rejection. Urinalysis revealed 100 uric acid crystal particles. The blood chemistry test results showed rapid increases in serum creatinine (from 2.86 mg/dL to 5.58 mg/dL) and 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 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 the 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. 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.

中文翻译:

患有基础再生障碍性贫血的肾移植受者在抗胸腺细胞球蛋白治疗后急性肾损伤伴极度高尿酸血症:病例报告。

抗胸腺细胞球蛋白治疗后高尿酸血症和急性肾损伤的发生在肾移植受者中并不常见。在这里,我们报告了一例患有基础再生障碍性贫血的肾移植受者在抗胸腺细胞球蛋白治疗后出现急性肾损伤伴极度高尿酸血症的病例。一名 40 岁的再生障碍性贫血女性在 5 年 6 个月前接受了肾移植,在接受抗胸腺细胞球蛋白治疗急性 T 细胞介导的抗胸腺细胞球蛋白治疗 6 天后,因少尿、全身水肿和全身无力到我们急诊科就诊。拒绝。尿液分析显示有 100 个尿酸结晶颗粒。血液化学测试结果显示血清肌酐(从 2.86 mg/dL 到 5.58 mg/dL)和尿酸水平(从 10.2 mg/dL 到 32.7 mg/dL)迅速增加,提示急性尿酸性肾病。怀疑肿瘤溶解综合征是急性尿酸性肾病的原因;因此,该患者被重新评估为再生障碍性贫血。人白细胞抗原-DR15 呈阳性,流式细胞术显示糖磷脂酰肌醇缺乏的粒细胞比例较低(2.9%),提示阵发性夜间血红蛋白尿克隆。这些发现表明,先前诊断出的再生障碍性贫血要么最初是低细胞骨髓增生异常综合征 (MDS),要么后来转变为低细胞 MDS,这是一种骨髓衰竭综合征。临床医生应将意外的肿瘤溶解综合征视为具有潜在骨髓衰竭综合征的肾移植受者抗胸腺细胞球蛋白治疗后并发症的原因。
更新日期:2020-07-02
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