血液学稳定的尿毒症患者的基线红细胞生成率和控制。

A J Erslev, A Besarab
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引用次数: 0

摘要

一般认为,尿毒症的贫血是由促红细胞生成素的产生减少引起的。然而,红细胞生成素滴度不低于而等于或高于正常非贫血个体。为了检验这种差异,我们对22例血液学稳定的透析患者进行了红细胞动力学研究,这些患者没有临床或实验室证据表明存在肾外炎症、感染或肿瘤疾病。14岁的红细胞寿命正常,由于红细胞比容稳定,他们每天的红细胞生成速度必须等于每天的红细胞破坏速度,这可以通过红细胞质量除以红细胞寿命来确定。尽管红细胞生成素滴度相同或更高,但这些比率约为正常稳定个体的一半。这提示尿毒症的贫血部分是由于骨髓对内源性促红细胞生成素的反应降低引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The rate and control of baseline red cell production in hematologically stable patients with uremia.

It is generally accepted that the anemia of uremia is caused by decreased production of erythropoietin. Nevertheless, the erythropoietin titers are not lower than but equal to or higher than in normal non-anemic individuals. To examine this discrepancy, erythrokinetic studies were made of 22 hematologically stable dialysis patients without clinical or laboratory evidence of extrarenal inflammation, infection, or neoplastic disorders. The red cell life span was normal in 14, and because of stable hematocrits, their daily rate of red cell production had to equal their daily rate of red cell destruction, which could be determined by dividing the red cell mass by red cell life span. These rates were about one half the rates of normal stable individuals, despite the same or higher erythropoietin titers. This suggests that the anemia of uremia is caused in part by a decreased bone marrow response to endogenous erythropoietin.

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