CD44作为早期检测肾移植后钙调磷酸酶抑制剂引起的肾毒性的病理标志物。

IF 1.3 4区 医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL
Asako Hayashi, Takayuki Okamoto, Junko Nio-Kobayashi, Naoya Iwahara, Ryota Suzuki, Yasuhiro Ueda, Toshiyuki Takahashi, Yasuyuki Sato, Toshihiko Iwanaga, Kiyohiko Hotta
{"title":"CD44作为早期检测肾移植后钙调磷酸酶抑制剂引起的肾毒性的病理标志物。","authors":"Asako Hayashi,&nbsp;Takayuki Okamoto,&nbsp;Junko Nio-Kobayashi,&nbsp;Naoya Iwahara,&nbsp;Ryota Suzuki,&nbsp;Yasuhiro Ueda,&nbsp;Toshiyuki Takahashi,&nbsp;Yasuyuki Sato,&nbsp;Toshihiko Iwanaga,&nbsp;Kiyohiko Hotta","doi":"10.2220/biomedres.43.181","DOIUrl":null,"url":null,"abstract":"<p><p>Long-term calcineurin inhibitor (CNI) administration causes irreversible nephrotoxicity. Therefore, early CNI-induced nephrotoxicity detection is necessary for patients who will need long-term CNI administration. There is no pathological indicator for early CNI-induced nephrotoxicity. Here, serial protocol kidney biopsy specimens from five kidney-transplant patients with severe CNI-induced nephrotoxicity were examined. We observed that the increase in CD44 expression in glomerular parietal epithelial cells (PECs) preceded the chronic pathological changes of CNI-induced nephrotoxicity such as tubular atrophy/interstitial fibrosis, arterial hyaline thickening, and focal segmental glomerulosclerosis (FSGS). This result suggests that CD44-positive PECs have pivotal roles in FSGS development in human CNI-induced nephrotoxicity as well as rodent models. CD44 could be useful as a pathological marker for early CNI-induced nephrotoxicity detection post kidney transplantation.</p>","PeriodicalId":9138,"journal":{"name":"Biomedical Research-tokyo","volume":null,"pages":null},"PeriodicalIF":1.3000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"CD44 as a pathological marker for the early detection of calcineurin inhibitor-induced nephrotoxicity post kidney transplantation.\",\"authors\":\"Asako Hayashi,&nbsp;Takayuki Okamoto,&nbsp;Junko Nio-Kobayashi,&nbsp;Naoya Iwahara,&nbsp;Ryota Suzuki,&nbsp;Yasuhiro Ueda,&nbsp;Toshiyuki Takahashi,&nbsp;Yasuyuki Sato,&nbsp;Toshihiko Iwanaga,&nbsp;Kiyohiko Hotta\",\"doi\":\"10.2220/biomedres.43.181\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Long-term calcineurin inhibitor (CNI) administration causes irreversible nephrotoxicity. Therefore, early CNI-induced nephrotoxicity detection is necessary for patients who will need long-term CNI administration. There is no pathological indicator for early CNI-induced nephrotoxicity. Here, serial protocol kidney biopsy specimens from five kidney-transplant patients with severe CNI-induced nephrotoxicity were examined. We observed that the increase in CD44 expression in glomerular parietal epithelial cells (PECs) preceded the chronic pathological changes of CNI-induced nephrotoxicity such as tubular atrophy/interstitial fibrosis, arterial hyaline thickening, and focal segmental glomerulosclerosis (FSGS). This result suggests that CD44-positive PECs have pivotal roles in FSGS development in human CNI-induced nephrotoxicity as well as rodent models. CD44 could be useful as a pathological marker for early CNI-induced nephrotoxicity detection post kidney transplantation.</p>\",\"PeriodicalId\":9138,\"journal\":{\"name\":\"Biomedical Research-tokyo\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biomedical Research-tokyo\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2220/biomedres.43.181\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical Research-tokyo","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2220/biomedres.43.181","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 2

摘要

长期服用钙调磷酸酶抑制剂(CNI)会引起不可逆的肾毒性。因此,对于需要长期使用CNI的患者,早期检测CNI引起的肾毒性是必要的。早期cni所致肾毒性没有病理指标。本文对5例严重cni所致肾毒性肾移植患者的肾活检标本进行了检查。我们观察到CD44在肾小球壁上皮细胞(PECs)中表达的增加,在cni引起的肾毒性的慢性病理改变(如小管萎缩/间质纤维化、动脉透明质增厚和局灶节段性肾小球硬化(FSGS)之前。这一结果表明,cd44阳性PECs在人类cni肾毒性和啮齿动物模型中FSGS的发展中起关键作用。CD44可作为肾移植后早期cni所致肾毒性检测的病理标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CD44 as a pathological marker for the early detection of calcineurin inhibitor-induced nephrotoxicity post kidney transplantation.

Long-term calcineurin inhibitor (CNI) administration causes irreversible nephrotoxicity. Therefore, early CNI-induced nephrotoxicity detection is necessary for patients who will need long-term CNI administration. There is no pathological indicator for early CNI-induced nephrotoxicity. Here, serial protocol kidney biopsy specimens from five kidney-transplant patients with severe CNI-induced nephrotoxicity were examined. We observed that the increase in CD44 expression in glomerular parietal epithelial cells (PECs) preceded the chronic pathological changes of CNI-induced nephrotoxicity such as tubular atrophy/interstitial fibrosis, arterial hyaline thickening, and focal segmental glomerulosclerosis (FSGS). This result suggests that CD44-positive PECs have pivotal roles in FSGS development in human CNI-induced nephrotoxicity as well as rodent models. CD44 could be useful as a pathological marker for early CNI-induced nephrotoxicity detection post kidney transplantation.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Biomedical Research-tokyo
Biomedical Research-tokyo 医学-医学:研究与实验
CiteScore
2.40
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Biomedical Research is peer-reviewed International Research Journal . It was first launched in 1990 as a biannual English Journal and later became triannual. From 2008 it is published in Jan-Apr/ May-Aug/ Sep-Dec..
×
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