血液透析患者皮肤瘙痒发病机制的研究进展
Research Progress on Pathogenesis of Skin Pruritus in Patients with Hemodialysis
DOI: 10.12677/md.2026.161012, PDF,   
作者: 潘彤彤*:济宁医学院临床医学院(附属医院),山东 济宁;李新建#:济宁医学院附属医院(临床医学院)肾内科,山东 济宁
关键词: 慢性肾脏病相关性瘙痒血液透析尿毒症性瘙痒症发病机制Chronic Kidney Disease-Associated Pruritus (CKD-aP) Hemodialysis Uremic Pruritus (UP) Pathogenesis
摘要: 慢性肾脏病相关性瘙痒(CKD-associated Pruritus, CKD-aP),又称尿毒症性瘙痒症(Uremic Pruritus, UP),是维持性血液透析患者常见的并发症,严重影响患者的生活质量,并与不良预后相关。其在血液透析患者中的患病率高达22%~84%。尽管近20年来透析技术不断进步,但中重度瘙痒的患病率仍维持在20%~40%。目前研究表明,CKD-aP的发病机制涉及多因素交互作用:皮肤干燥症通过破坏皮肤屏障、降低瘙痒阈值加剧症状;免疫炎症失调表现为辅助性T细胞1 (T helper 1 cell, Th1)、白细胞介素-6 (Interleukin-6, IL-6)、白细胞介素-31 (Interleukin-31, IL-31)等炎症因子升高,驱动系统性炎症反应;μ-阿片受体(μ-Opioid Receptor, MOR)过度激活与κ-阿片受体(κ-Opioid Receptor, KOR)表达减少,打破瘙痒调节平衡;尿毒症毒素(如硫酸吲哚酚、甲状旁腺激素、磷酸钙等)累积直接或间接激活神经纤维与炎症通路;神经系统紊乱涉及瞬时受体电位香草酸亚型1 (Transient Receptor Potential Vanilloid 1, TRPV1)、T型钙通道亚型Cav3.2 (Cav3.2)等离子通道异常及神经营养因子失衡,导致瘙痒信号传导异常。此外,环境污染物及个体差异等亦参与发病。尽管现有证据揭示了多维度机制,但各因素间的协同作用仍需深入探索,这为开发针对性的治疗策略提供了潜在方向。
Abstract: Chronic Kidney Disease-associated pruritus (CKD-aP), also known as Uremic Pruritus (UP), is a common complication in patients undergoing maintenance hemodialysis, significantly impairing quality of life and associated with poor prognosis. Its prevalence among hemodialysis patients ranges from 22% to 84%. Despite advances in dialysis technology over the past two decades, the prevalence of moderate to severe pruritus remains between 20% and 40%. Current evidence indicates that the pathogenesis of CKD-aP involves multiple interacting factors: xerosis cutis exacerbates symptoms by disrupting the skin barrier and lowering the itch threshold; immune-inflammatory dysregulation manifests as elevated inflammatory factors such as T helper 1 (Th1) cells, Interleukin-6 (IL-6), and Interleukin-31 (IL-31), driving systemic inflammatory responses; imbalance in the opioid system, characterized by overactivation of μ-Opioid Receptors (MOR) and reduced expression of κ-Opioid Receptors (KOR), disrupts the equilibrium of itch modulation; accumulation of uremic toxins (e.g., indoxyl sulfate, parathyroid hormone, calcium-phosphate complexes) directly or indirectly activates nerve fibers and inflammatory pathways; nervous system dysregulation involves abnormalities in ion channels such as transient receptor potential vanilloid 1 (TRPV1) and Cav3.2, along with imbalances in neurotrophic factors, leading to aberrant itch signaling. Furthermore, environmental pollutants and individual differences also contribute to disease manifestation. Although existing evidence highlights multidimensional mechanisms, the synergistic interactions among these factors warrant further investigation, offering potential directions for developing targeted therapeutic strategies.
文章引用:潘彤彤, 李新建. 血液透析患者皮肤瘙痒发病机制的研究进展[J]. 医学诊断, 2026, 16(1): 80-90. https://doi.org/10.12677/md.2026.161012

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