慢性尿毒症时的血液学变化

来源 :国外医学.泌尿系统分册 | 被引量 : 0次 | 上传用户:hw0303
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血液透析治疗延长了肾病终末期病人的生命,近年来对于慢性肾功能不全引起的并发症逐渐予以重视。肾功能不全重大的并发症之一是慢性尿毒症对血细胞组成成份的影响,肾性贫血应放在首位,因为它是影响康复的因素。肾性贫血大多数是正常色素和正常红细胞贫血。并由三种不同组成部分构成:再生障碍性贫血,溶血性贫血和慢性出血性贫血。在慢性肾功能不全时,三者中的任何一种症状均可首先单独出现。以再生障碍为原因的肾性贫血缺乏红细胞生成素:五十年代末就已经知道不仅慢性肾病,而肾切也会减少红细胞形成,且对红细胞形成刺激剂无效,由于结扎输尿管引起的红细胞形成障碍相对地好得多。后来发现肾脏由产生一种因素直接或经过血浆蛋白起作用,刺激红细胞生成,按目前的看法这个因素是分子量在30000~70000之间的醣蛋白,在肾功能障碍终末期时红细胞生成素的分解明显延迟,但这并不能使尿毒症患者红细胞生成素的缺乏达到均衡。 Hemodialysis treatment prolongs the life of patients with end-stage renal disease, and in recent years, more attention has been paid to the complications caused by chronic renal insufficiency. One of the major complications of renal insufficiency is the effect of chronic uremia on the composition of blood cells, renal anemia should be placed in the first place, because it is a factor that affects rehabilitation. Most renal anemia is normal pigment and normal red blood cell anemia. It consists of three distinct components: aplastic anemia, hemolytic anemia and chronic hemorrhagic anemia. In chronic renal failure, any of the three symptoms can be the first to appear alone. Renal anemia, a cause of aplastic anemia, lacks erythropoietin: In the late 1950s, not only chronic kidney disease was known, but nephrectomy also reduced the formation of erythrocytes and was ineffective in stimulating erythrocytes, causing disorders in the formation of erythrocytes due to ligation of the ureters Relatively much better. Later found that the kidneys by producing a factor directly or through plasma proteins to stimulate erythropoiesis, the current view of this factor is the molecular weight between 30000 ~ 70000 glycoprotein, end of renal dysfunction, erythropoietin decomposition Obvious delay, but this does not make the lack of erythropoietin uremia in patients with equilibrium.
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