Erslev A J, Besarab A
Cardeza Foundation, Philadelphia, PA 19107, USA.
J Lab Clin Med. 1995 Sep;126(3):283-6.
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.
一般认为,尿毒症性贫血是由促红细胞生成素生成减少所致。然而,尿毒症患者促红细胞生成素水平并不低于正常非贫血个体,而是等于或高于正常非贫血个体。为研究这一差异,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,这些患者无肾外炎症、感染或肿瘤性疾病的临床或实验室证据。14例患者的红细胞寿命正常,由于血细胞比容稳定,其红细胞每日生成率必须等于每日红细胞破坏率,后者可通过红细胞量除以红细胞寿命来确定。尽管促红细胞生成素水平相同或更高,但这些患者的红细胞生成率约为正常稳定个体的一半。这表明,尿毒症性贫血部分是由骨髓对内源性促红细胞生成素反应降低所致。