Koch K M, Radtke H W
Klin Wochenschr. 1979 Oct 1;57(19):1031-6. doi: 10.1007/BF01479988.
A review is given of clinical studies performed by use of a highly sensitive in-vitro erythropoietin assay (fetal mouse livercell culture) in large patients' populations to clarify the controversial role of erythropoietin deficiency in the pathogenesis of renal anemia. Studies involved a.) patients with chronic renal disease and varying degree of renal insufficiency in the predialysis phase b.) non-nephrectomized and anephric patients on regular hemodialysis treatment. The data available demonstrate that the initial phase of renal anemia is accompanied by a compensatory increase of serumerythropoietin concentration and therefore erythropoietin deficiency has to be excluded as a primary cause of the anemia of renal failure; merely a relative lack of erythropoietin seems to exist. In the terminal phase of renal failure, erythropoietin deficiency becomes absolute, such in 50% of the investigated non-nephrectomized hemodialysis patients and in all anephric patients. However in individual patients even in terminal renal failure a sustained regulatory feedback mechanism between serumerythropoietin concentration and hematocrit, probably working at lower hematocrit level, could be demonstrated.
本文综述了在大量患者群体中使用高灵敏度体外促红细胞生成素检测法(胎鼠肝细胞培养)进行的临床研究,以阐明促红细胞生成素缺乏在肾性贫血发病机制中的争议性作用。研究涉及:a. 处于透析前阶段、患有慢性肾病且肾功能不全程度各异的患者;b. 接受定期血液透析治疗的未行肾切除术和无肾患者。现有数据表明,肾性贫血的初始阶段伴随着血清促红细胞生成素浓度的代偿性升高,因此必须排除促红细胞生成素缺乏作为肾衰竭贫血的主要原因;似乎仅存在相对的促红细胞生成素缺乏。在肾衰竭的终末期,促红细胞生成素缺乏变为绝对缺乏,在50%的接受调查的未行肾切除术的血液透析患者和所有无肾患者中均如此。然而,即使在个别终末期肾衰竭患者中,也能证明血清促红细胞生成素浓度与血细胞比容之间存在持续的调节反馈机制,该机制可能在较低的血细胞比容水平起作用。