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再生障碍性贫血肾移植受者应用抗胸腺细胞球蛋白治疗后发生急性肾损伤伴极度高尿酸血症:病例报告。

Acute kidney injury with extreme hyperuricemia after antithymocyte globulin treatment in a kidney transplant recipient with underlying aplastic anemia: a case report.

机构信息

Division of Nephrology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul, 06591, South Korea.

出版信息

BMC Nephrol. 2020 Jul 2;21(1):251. doi: 10.1186/s12882-020-01903-9.

DOI:10.1186/s12882-020-01903-9
PMID:32615929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7330935/
Abstract

BACKGROUND

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.

CASE PRESENTATION

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.

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.

摘要

背景

在接受抗胸腺细胞球蛋白治疗的肾移植受者中,高尿酸血症和急性肾损伤的发生并不常见。在此,我们报告了一例由再生障碍性贫血引起的独特病例,该患者在接受抗胸腺细胞球蛋白治疗急性 T 细胞介导的排斥反应后出现了严重的高尿酸血症和急性肾损伤。

病例介绍

一名 40 岁女性,因再生障碍性贫血于 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后 6 天因急性 T 细胞介导的排斥反应出现少尿、全身水肿和全身无力,到我院急诊科就诊。尿分析显示 100 个尿酸晶体颗粒。血液化学检测结果显示血清肌酐(从 2.86mg/dL 增加到 5.58mg/dL)和尿酸水平(从 10.2mg/dL 增加到 32.7mg/dL)迅速升高,提示急性尿酸肾病。怀疑肿瘤溶解综合征是导致急性尿酸肾病的原因;因此,重新评估了该患者的再生障碍性贫血。人类白细胞抗原-DR15 阳性,流式细胞术显示糖磷脂酰肌醇缺陷粒细胞的比例低(2.9%),提示阵发性睡眠性血红蛋白尿克隆。这些发现表明,之前诊断的再生障碍性贫血原本可能是低细胞性骨髓增生异常综合征(MDS),或者后来转化为低细胞性 MDS,这是一种骨髓衰竭综合征。

结论

对于有潜在骨髓衰竭综合征的肾移植受者,在接受抗胸腺细胞球蛋白治疗后出现并发症时,临床医生应考虑意外的肿瘤溶解综合征是其病因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b29e/7330935/93a8745bf175/12882_2020_1903_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b29e/7330935/cd19be57199d/12882_2020_1903_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b29e/7330935/93a8745bf175/12882_2020_1903_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b29e/7330935/cd19be57199d/12882_2020_1903_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b29e/7330935/93a8745bf175/12882_2020_1903_Fig2_HTML.jpg

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Prediction of mizoribine pharmacokinetic parameters by serum creatinine in renal transplant recipients.血清肌酐对肾移植受者米唑立宾药代动力学参数的预测
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