Evaluation of molecular profiles in calcineurin inhibitor toxicity post-kidney transplant: input to chronic allograft dysfunction.
Evaluation of molecular profiles in calcineurin inhibitor toxicity post-kidney transplant: input to chronic allograft dysfunction.
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DOI：
10.1111/ajt.12696
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发表时间：
2014-05
期刊：
影响因子：
--
通讯作者：
Mas VR
中科院分区：
文献类型：
--
作者：
Maluf DG;Dumur CI;Suh JL;Lee JK;Cathro EP;King AL;Gallon L;Brayman KL;Mas VR
肾移植(KT)中钙调神经磷酸酶抑制剂毒性(CNIT)的分子基础及其在慢性移植物功能障碍(CAD)间质纤维化(IF)和肾小管萎缩(TA)中的作用通过以下两个方面进行评估：1)确定与移植物损伤相关的特定CNIT分子通路(横断面研究)；2)通过IF/TA纵向研究(IF/TA)评估CNIT信号在进展为CAD中的作用。对组织学诊断为CNIT(n=14)、急性排斥(AR，n=13)和CAD合并IF/TA(n=10)的肾移植受者的肾活检进行评估。正常同种异体肾移植组(NA，n=18)作为对照。为了测试CNIT对CAD进展的贡献，对61例KT患者在KT后3个月和~12个月(范围=9-18)收集的一组独立的活检(n=122)进行了评估。根据移植后2年的功能和组织学结果，患者被分为进展组(n=30)和非进展组(n=31)。鉴定了表征CNIT样品的分子特征。进展患者在KT后3个月和~12个月分别与CNIT信号有7%和22%的重叠，而在非进展患者中CNIT信号的重叠分别为1%和1%，在分子水平上表明CNIT是参与进展到CAD的非免疫因素。
The molecular basis of calcineurin inhibitor toxicity (CNIT) in kidney transplantation (KT) and its contribution to chronic allograft dysfunction (CAD) with interstitial fibrosis (IF) and tubular atrophy (TA) were evaluated by: 1) identifying specific CNIT molecular pathways that associate with allograft injury (cross-sectional study), and 2) assessing the contribution of the identified CNIT signature in the progression to CAD with IF/TA (longitudinal study). Kidney biopsies from well-selected transplant recipients with histological diagnosis of CNIT (n=14), acute rejection (AR, n=13), and CAD with IF/TA (n=10) were evaluated. Normal allografts (NA, n=18) were used as controls. To test CNIT contribution to CAD progression, an independent set of biopsies (n=122) from 61 KT patients collected at 3 and at ~12 months post-KT (range=9-18) were evaluated. Patients were classified based on 2-year post-KT graft function and histological findings as progressors (n=30) or non-progressors to CAD (n=31). Molecular signatures characterizing CNIT samples were identified. Patients classified as progressors showed an overlap of 7% and 22% with the CNIT signature at 3 and at ~12 months post-KT respectively, while the overlap was <1% and 1% in non-progressors patients, showing CNIT at the molecular level as a non-immunological factor involved in the progression to CAD.
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影响因子：
3.8
作者：
Cui, Yuxia;Huang, Qihong;Paules, Richard S.
通讯作者：
Paules, Richard S.
影响因子：
8.8
作者：
Famulski, K. S.;Broderick, G.;Halloran, P. F.
通讯作者：
Halloran, P. F.
DOI：
10.1111/j.2517-6161.1995.tb02031.x
发表时间：
1995-01-01
影响因子：
5.8
作者：
BENJAMINI, Y;HOCHBERG, Y
通讯作者：
HOCHBERG, Y
影响因子：
6.1
作者：
Glowacki, Francois;Lionet, Arnaud;Cauffiez, Christelle
通讯作者：
Cauffiez, Christelle
影响因子：
6.2
作者：
Heidt, Sebastiaan;Roelen, Dave L.;Mulder, Arend
通讯作者：
Mulder, Arend