Hotta T, Maeda H, Suzuki I, Chung T G, Saito A
Proc Soc Exp Biol Med. 1987 Oct;186(1):47-51. doi: 10.3181/00379727-186-42582.
The pathogenesis of anemia in patients with chronic renal failure was studied by analyzing the effect of uremic sera on the in vitro colony growth of erythroid (CFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells. Uremic sera from 20 of 30 patients inhibited erythroid colony growth below 70% of control even when cultured with normal human bone marrow of the same blood type. On the other hand, only one of the sera inhibited colony growth of CFU-GM as compared with normal sera. On Sephadex G-15 gel filtration, the CFU-E-inhibiting activity appeared in two different fractions: the void volume peak and the delayed eluant before the second peak. The inhibiting activity in the former fraction was noted only in uremic sera. The results of this study suggest the existence of a serum inhibitor(s) of erythropoiesis with a relative molecular mass of more than 1500 Da which are virtually impossible to dialyze by conventional membranes.
通过分析尿毒症血清对红系祖细胞（CFU-E）和粒-巨噬系祖细胞（CFU-GM）体外集落生长的影响，研究了慢性肾衰竭患者贫血的发病机制。30例患者中20例的尿毒症血清即使与同血型正常人骨髓共同培养，也会使红系集落生长抑制至对照的70%以下。另一方面，与正常血清相比，只有一份血清抑制CFU-GM的集落生长。在Sephadex G-15凝胶过滤中，CFU-E抑制活性出现在两个不同的组分中：空体积峰和第二个峰之前的延迟洗脱液。前一组分中的抑制活性仅在尿毒症血清中出现。本研究结果提示存在一种相对分子质量超过1500 Da的血清红细胞生成抑制剂，这种抑制剂实际上不可能被传统膜透析。
