慢性肾脏病相关性瘙痒症(CKD-aP)的发病机制:理论模型与治疗相关性。

IF 3.2 Q1 UROLOGY & NEPHROLOGY Kidney360 Pub Date : 2024-09-04 DOI:10.34067/KID.0000000573
Frank Brennan
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引用次数: 0

摘要

我们对尿毒症性瘙痒症(又称慢性肾脏病相关性瘙痒症(CKD-aP))的发病机理仍然一无所知。虽然已经描述了 CKD-aP 患者皮肤免疫-化学环境的多种离散变化,但却缺乏一个连贯的机制理论。本文提出了一个机制理论模型。该模型集中于 CKD-aP 的起始阶段及其三个部分:1) 由最初的诱发因素引发的起始阶段;2) 随后的细胞因子级联释放以及多个皮肤细胞之间和传入神经纤维之间的交叉对话;3) 增强阶段。将说明该模型的局限性,并提出未来研究的设想。还将探讨对管理的影响。
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The Pathogenesis of CKD - Associated Pruritus (CKD-aP): A Theoretical Model and Relevance for Treatment.

Our understanding of the pathogenesis of uremic pruritus (also known as Chronic Kidney Disease - associated pruritus (CKD-aP)) remains elusive. While multiple discrete changes in the immuno-chemical milieu of the skin of patients with CKD-aP have been described, a coherent theory of mechanism is absent. This article proposes a theoretical model of mechanism. It concentrates on the initiation phase of CKD-aP and its three parts: 1) Genesis, triggered by first precipitants; 2) Cascade of cytokine release that follows and the cross-talking of multiple skin cells with each other and afferent nerve fibers and 3) Enhancement. The limitation of the model will be described and ideas for future research proposed. Implications for management shall be examined.

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来源期刊
Kidney360
Kidney360 UROLOGY & NEPHROLOGY-
CiteScore
3.90
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