Shainkin-Kestenbaum R, Winikoff Y, Dvilansky A, Chaimovitz C, Nathan I
Nephron. 1986;44(4):295-8. doi: 10.1159/000184009.
The 'uremic toxin', guanidino propionic acid (GPA), which was detected in uremic serum in correlation with BUN level, modified the mitogenic response of normal lymphocytes to phytohemagglutinin (PHA). Mild modifications can be detected in the concentrations which are found in uremic patients. Other guanidino compounds which have been detected in uremic sera, such as guanidino succinic acid (GSA), guanidino butyric acid (GBA) and guanidino acetic acid (GAA), show similar inhibitory pathways. It is suggested that guanidino compounds contribute to the immunological disturbances in uremia. The complexity of their action on lymphocyte mitogenic response is probably the cause of the conflicting results which have been reported in the literature.
在尿毒症血清中检测到的与血尿素氮水平相关的“尿毒症毒素”——胍基丙酸（GPA），改变了正常淋巴细胞对植物血凝素（PHA）的促有丝分裂反应。在尿毒症患者体内发现的浓度下可检测到轻微变化。在尿毒症血清中检测到的其他胍基化合物，如胍基琥珀酸（GSA）、胍基丁酸（GBA）和胍基乙酸（GAA），显示出类似的抑制途径。有人提出胍基化合物促成了尿毒症中的免疫紊乱。它们对淋巴细胞促有丝分裂反应作用的复杂性可能是文献中报道结果相互矛盾的原因。
