Drug-induced Fanconi syndrome in patients with kidney allograft transplantation.

Drug-induced Fanconi syndrome in patients with kidney allograft transplantation.
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同种异体肾移植患者药物诱发的范可尼综合征。

DOI:
10.3389/fimmu.2022.979983
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发表时间:
2022
影响因子:
7.3
通讯作者:
Peng, Longkai
Peng, Longkai
中科院分区:
医学2区
文献类型:
--
作者:
Tang, Zhouqi;Li, Tengfang;Dai, Helong;Feng, Chen;Xie, Xubiao;Peng, Fenghua;Lan, Gongbin;Yu, Shaojie;Wang, Yu;Fang, Chunhua;Nie, Manhua;Yuan, Xiaoqiong;Tang, Xiaotian;Jiang, Xin;Zhu, Xuejing;Fan, Yuxi;Peng, Jiawei;Sun, Siyu;Zhong, Mingda;Zhang, Hedong;Peng, Longkai

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肾移植后的患者需要长期服用免疫抑制剂等药物。其中一些药物副作用容易与范可尼综合征的症状相混淆,造成误诊和漏诊,给患者造成严重后果。因此,提高对肾移植术后范可尼综合征的认识,早期诊断和治疗至关重要。本回顾性研究分析了中南大学湘雅二医院2016年7月至2021年1月收治的1728例异基因肾移植患者。对两名继发于药物阿德福韦酯(ADV)和他克莫司的范可尼综合征患者进行了筛查。我们总结了诊断过程,临床资料和预后。肾移植术后ADV继发Fanconi综合征发病隐匿,长期用药(>10年)后发病。晚期主要表现为骨痛、骨软化、脊柱侧凸,并伴有明显的近端肾小管损害(严重低磷血症、低钾血症、低钙血症、低尿酸血症、糖尿、蛋白尿、酸中毒等)。和肾功能损害(肌酐增加和氮质血症)。病理学表现为肾小管上皮细胞线粒体肿胀、变形。停药后上述症状和体征缓解,但脊柱侧凸难以矫正。继发于他克莫司的范可尼综合征有一个单一的表现,肌酐升高,这很容易与他克莫司肾毒性混淆。但是,减少他克罗莫司的剂量往往无效,在疾病发展的后期可以发现近端肾功能衰竭。骨代谢指标及影像学检查未见异常。当免疫抑制剂从他克莫司改为环孢素A时,肌酐水平迅速下降,近端肾小管功能恢复正常,未发生严重电解质失衡或尿成分丢失。首次报道了肾移植后药物诱导的范可尼综合征。这些结果证实,肾移植术后长期使用ADV或他克莫司可能会产生严重后果,其中一些是不可逆的。为了避免误诊和漏诊,有必要对肾移植后范可尼综合征有更深入的了解。
Patients after kidney transplantation need to take long-term immunosuppressive and other drugs. Some of these drug side effects are easily confused with the symptoms of Fanconi syndrome, resulting in misdiagnosis and missed diagnosis, and causing serious consequences to patients. Therefore, improving awareness, early diagnosis and treatment of Fanconi syndrome after kidney transplantation is critical. This retrospective study analyzed 1728 cases of allogeneic kidney transplant patients admitted to the Second Xiangya Hospital of Central South University from July 2016 to January 2021. Two patients with Fanconi syndrome secondary to drugs, adefovir dipivoxil (ADV) and tacrolimus, were screened. We summarized the diagnostic process, clinical data, and prognosis. The onset of Fanconi syndrome secondary to ADV after renal transplantation was insidious, and the condition developed after long-term medication (>10 years). It mainly manifested as bone pain, osteomalacia, and scoliosis in the late stage and was accompanied by obvious proximal renal tubular damage (severe hypophosphatemia, hypokalemia, hypocalcemia, hypouricemia, glycosuria, protein urine, acidosis, etc.) and renal function damage (increased creatinine and azotemia). The pathological findings included mitochondrial swelling and deformity in renal tubular epithelial cells. The above symptoms and signs were relieved after drug withdrawal, but the scoliosis was difficult to rectify. Fanconi syndrome secondary to tacrolimus has a single manifestation, increased creatinine, which can be easily confused with tacrolimus nephrotoxicity. However, it is often ineffective to reduce the dose of tacrolomus, and proximal renal failure can be found in the later stage of disease development. There was no abnormality in the bone metabolism index and imageological examination findings. The creatinine level decreased rapidly, the proximal renal tubule function returned to normal, and no severe electrolyte imbalance or urinary component loss occurred when the immunosuppression was changed from tacrolimus to cyclosporine A. For the first time, drug-induced Fanconi syndrome after kidney transplantation was reported. These results confirmed that the long-term use of ADV or tacrolimus after kidney transplantation may have serious consequences, some of which are irreversible. Greater understanding of Fanconi syndrome after kidney transplantation is necessary in order to avoid incorrect and missed diagnosis.
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