Department of Nephrology, St George Hospital, Sydney, New South Wales, Australia.
Kidney360. 2024 Nov 1;5(11):1727-1738. doi: 10.34067/KID.0000000573. Epub 2024 Sep 4.
Our understanding of the pathogenesis of uremic pruritus (also known as CKD-associated pruritus [CKD-aP]) remains elusive. Although multiple discrete changes in the immunochemical 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.
我们对尿毒症瘙痒(也称为 CKD 相关瘙痒[CKD-aP])的发病机制仍然难以理解。尽管已经描述了 CKD-aP 患者皮肤免疫化学环境中的多种离散变化,但缺乏连贯的机制理论。本文提出了一种机制理论模型。它集中在 CKD-aP 的启动阶段及其三个部分:(1)由最初的诱因引发的起源;(2)随后细胞因子释放的级联反应以及多种皮肤细胞之间的相互作用以及传入神经纤维;(3)增强。将描述模型的局限性,并提出未来研究的想法。将检查管理的意义。