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[尿毒症毒性的临床和代谢后果]

[Clinical and metabolic consequences of uremic toxicity].

作者信息

Rutkowski Przemysław

机构信息

Klinika Nefrologii Transplantologii i Chorób, Wewnetrznych Akademii Medycznej w Gdarsku.

出版信息

Przegl Lek. 2006;63(4):209-17.

PMID:17080744
Abstract

Retention of many substances takes place in the pathogenesis of uremic toxicity. There are almost 100 different molecules described and defined as uremic toxins. These substances are divided into three groups according to EUTOX group calssification. Small water soluble molecules with a molecular weight less than 500 D are included into the first group. Derivate of guanidines, purines, pyrimidines and methyloamines appeared in this group. There is also an unclassified subgroup with urea as a "classical" toxin which the real role in the uraemic syndrome is still discussed. Main symptoms caused by these molecules are digestive disturbances, neurological changes, hypertension etc. We can eliminate almost all of these toxins with standard methods used during dialysotherapy. Substances with a different molecular weight but connected with proteins determine the second group. AGE-s, phenol derivates, leptin and poliamines beside others create this group. There are many studies that have proved that these toxins cause hypertension, arteriosclerosis and shortened life time of hemodialysed patients. However, melatonin toxicity is not fully proved. Different types of renal replacement therapy are not valid to purify blood from protein-bound substances. Middle molecules are included into the third group, with a molecular weight higher than 500 D. There are cytokines, neuro-transmitters e.g. beta-endorphin, metencephalin and many others accounted into this group. One of them is the parathormon, well known and considered as "universal" toxin for several years. Middle molecules are causing very different effects. They are responsible for: anemia, arteriosclerosis, chronic inflammation and generally increase dialysed patient mortality. Toxic action of several molecules described below is still not proved; however there are some ongoing studies aimed to find pathophysiological links between old and new described uremic toxins.

摘要

许多物质的潴留发生在尿毒症毒性的发病机制中。几乎有100种不同的分子被描述和定义为尿毒症毒素。根据EUTOX组分类,这些物质分为三组。第一组包括分子量小于500 D的小水溶性分子。胍类、嘌呤类、嘧啶类和甲基胺类的衍生物出现在这一组中。还有一个未分类的亚组,以尿素作为“经典”毒素,其在尿毒症综合征中的真正作用仍在讨论中。这些分子引起的主要症状是消化紊乱、神经变化、高血压等。我们可以用透析治疗中使用的标准方法消除几乎所有这些毒素。分子量不同但与蛋白质相关的物质构成第二组。晚期糖基化终末产物、酚类衍生物、瘦素和多胺等构成了这一组。许多研究已经证明,这些毒素会导致高血压、动脉硬化和血液透析患者寿命缩短。然而,褪黑素毒性尚未得到充分证实。不同类型 的肾脏替代疗法对清除血液中的蛋白质结合物质无效。第三组包括中分子,分子量高于500 D。细胞因子、神经递质如β-内啡肽、脑啡肽等都属于这一组。其中之一是甲状旁腺激素,多年来一直被认为是“通用”毒素。中分子会产生非常不同的影响。它们导致:贫血、动脉硬化、慢性炎症,并总体上增加透析患者的死亡率。下面描述的几种分子的毒性作用尚未得到证实;然而,有一些正在进行的研究旨在寻找新旧描述的尿毒症毒素之间的病理生理联系。

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