New Onset Diabetic Ketoacidosis in a Renal Transplant Recipient.

Havird McLean Skalak, Kaitlyn Haas, Melissa Laub, Laura L Mulloy
{"title":"New Onset Diabetic Ketoacidosis in a Renal Transplant Recipient.","authors":"Havird McLean Skalak, Kaitlyn Haas, Melissa Laub, Laura L Mulloy","doi":"10.1016/j.amjms.2024.08.023","DOIUrl":null,"url":null,"abstract":"<p><p>Post-transplant diabetes mellitus (PTDM) is a well-known solid organ transplant complication, which can be related to immunosuppressants, particularly tacrolimus. We report an unusual presentation of PTDM with diabetic ketoacidosis (DKA). This is unique as PTDM typically resembles Type 2 DM, whereas DKA is associated with Type 1 DM and has rarely been reported as a complication of tacrolimus. A 38-year-old African American male on LCP-tacrolimus presented four months post kidney transplant with vomiting, weakness, poor appetite, and polyuria. Labs demonstrated hyperglycemia, ketonuria, and high anion gap metabolic acidosis. He was nonobese and had no personal or family history of Type 2 DM. DKA was suspected to be secondary to tacrolimus-induced pancreatic beta cell damage worsened by supratherapeutic tacrolimus levels. Latent autoimmune diabetes in adults (LADA) was diagnosed when further testing showed insulinopenia, low C-peptide, and anti-glutamic acid decarboxylase (GAD) autoantibodies. He required 120-units of subcutaneous insulin daily. Our literature review revealed only 16 other tacrolimus-induced DKA cases. No cases reported anti-GAD positivity and most showed beta cell toxicity reversibility with tacrolimus tapering or substitution. Our patient was early post-transplant with leukocytopenia, so tacrolimus was not exchanged. This unusual PTDM case may have resulted from both autoimmune and tacrolimus-induced beta cell destruction. Physicians should be aware of new onset LADA post-transplantation and tacrolimus toxicity leading to DKA, even in patients without traditional risk factors. Anti-GAD antibody screening in patients on tacrolimus who develop PTDM may identify patients less likely to recover beta cell function with immunosuppression augmentation which requires careful monitoring.</p>","PeriodicalId":94223,"journal":{"name":"The American journal of the medical sciences","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The American journal of the medical sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.amjms.2024.08.023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Post-transplant diabetes mellitus (PTDM) is a well-known solid organ transplant complication, which can be related to immunosuppressants, particularly tacrolimus. We report an unusual presentation of PTDM with diabetic ketoacidosis (DKA). This is unique as PTDM typically resembles Type 2 DM, whereas DKA is associated with Type 1 DM and has rarely been reported as a complication of tacrolimus. A 38-year-old African American male on LCP-tacrolimus presented four months post kidney transplant with vomiting, weakness, poor appetite, and polyuria. Labs demonstrated hyperglycemia, ketonuria, and high anion gap metabolic acidosis. He was nonobese and had no personal or family history of Type 2 DM. DKA was suspected to be secondary to tacrolimus-induced pancreatic beta cell damage worsened by supratherapeutic tacrolimus levels. Latent autoimmune diabetes in adults (LADA) was diagnosed when further testing showed insulinopenia, low C-peptide, and anti-glutamic acid decarboxylase (GAD) autoantibodies. He required 120-units of subcutaneous insulin daily. Our literature review revealed only 16 other tacrolimus-induced DKA cases. No cases reported anti-GAD positivity and most showed beta cell toxicity reversibility with tacrolimus tapering or substitution. Our patient was early post-transplant with leukocytopenia, so tacrolimus was not exchanged. This unusual PTDM case may have resulted from both autoimmune and tacrolimus-induced beta cell destruction. Physicians should be aware of new onset LADA post-transplantation and tacrolimus toxicity leading to DKA, even in patients without traditional risk factors. Anti-GAD antibody screening in patients on tacrolimus who develop PTDM may identify patients less likely to recover beta cell function with immunosuppression augmentation which requires careful monitoring.

肾移植受者新发糖尿病酮症酸中毒
移植后糖尿病(PTDM)是一种众所周知的实体器官移植并发症,可能与免疫抑制剂,尤其是他克莫司有关。我们报告了一种伴有糖尿病酮症酸中毒(DKA)的 PTDM 异常表现。这是一个独特的病例,因为 PTDM 通常类似于 2 型糖尿病,而 DKA 则与 1 型糖尿病有关,并且很少有作为他克莫司并发症的报道。一名服用 LCP-他克莫司的 38 岁非裔美国男性在肾移植术后四个月出现呕吐、乏力、食欲不振和多尿。实验室检查显示他患有高血糖、酮尿和高阴离子间隙代谢性酸中毒。他并不肥胖,也没有2型糖尿病的个人或家族病史。疑似继发于他克莫司诱发的胰腺β细胞损伤,而过高的他克莫司治疗水平又加重了胰腺β细胞损伤。当进一步检测发现胰岛素分泌减少、低C肽和抗谷氨酸脱羧酶(GAD)自身抗体时,他被诊断为成人潜伏性自身免疫性糖尿病(LADA)。他每天需要皮下注射 120 单位的胰岛素。我们查阅文献后发现,他克莫司诱发的 DKA 病例仅有 16 例。没有任何病例报告抗 GAD 阳性,大多数病例显示,他克莫司减量或替代后β细胞毒性可逆。我们的患者在移植后早期出现白细胞减少,因此没有更换他克莫司。这种不寻常的 PTDM 病例可能是由于自身免疫和他克莫司引起的β细胞破坏造成的。医生应注意移植后新发的 LADA 和他克莫司毒性导致的 DKA,即使患者没有传统的风险因素。在使用他克莫司并出现 PTDM 的患者中进行抗 GAD 抗体筛查,可以发现在加强免疫抑制的情况下不太可能恢复 β 细胞功能的患者,这就需要进行仔细监测。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信