Sivak L, Scuteri R M, Cavalli N H, Gotlieb D, López Blanco O A
Centro Integral de Nefrología y Trasplantes, Sanatorio Güemes, Buenos Aires, Argentina.
Medicina (B Aires). 1992;52(6):516-22.
The hematologic findings of chronic renal failure are consistent with hypoproliferative anemia; the pathogenesis of the anemia is primarily due to decreased erythropoietin production by the diseased kidneys. There are aggravating factors (AF) contributing to this primordial cause: inhibitors to erythroid marrow function, shortened red cell survival, nonevident chronic blood loss (owing to uremic platelet dysfunction), iron and/or folate deficiency, aluminium toxicity, hemolysis (acute or chronic), etc. Ten patients with end stage renal disease, treated with maintenance hemodialysis and high transfusional requirement (more than 300 ml/month) are presented; in five the AF were discarded by a previously presented protocol (Table 1) and they were treated with human recombinant erythropoietin (r-HuEPO) intravenously, in conventional schemes (three times a week) and doses (195 +/- 41 Units/Kg)-Group A-. The AF were not studied in the other five and the r-HuEPO treatment employed different doses (125 +/- 70 U/K/W) and protocols (1.7 +/- 0.5 times a week)-Group B-(Table 2). The transfusional requirement disappeared and the hematocrit and the hemoglobin rose significantly in both groups (more in group A) (Table 3). The significant drop in ferritin levels (147 +/- 30 ng/ml vs 27.5 +/- 11 ng/ml at the 12th week) and the stabilization in reticulocyte count (1.4% at start vs 2% at 12th week) indicate iron consumption; in the meantime, the persistent increment in reticulocyte production index (1 at start vs 3 at 12th week) revealed a continuous stimulation of the erythropoiesis (Fig. 1). No clinical and/or vascular complications were observed; arterial pressure and serum potassium levels did not rise significantly so that r-HuEPO treatment was not canceled in any case.(ABSTRACT TRUNCATED AT 250 WORDS)
慢性肾衰竭的血液学表现与增生低下性贫血相符;贫血的发病机制主要是患病肾脏产生促红细胞生成素减少。有一些加重因素(AF)导致了这一原发性病因:红系骨髓功能抑制剂、红细胞存活时间缩短、隐匿性慢性失血(由于尿毒症性血小板功能障碍)、铁和/或叶酸缺乏、铝中毒、溶血(急性或慢性)等。本文报告了10例终末期肾病患者,他们接受维持性血液透析且输血需求量大(每月超过300毫升);其中5例通过先前提出的方案排除了加重因素(表1),并按照常规方案(每周3次)和剂量(195±41单位/千克)静脉注射重组人促红细胞生成素(r-HuEPO)——A组。另外5例未研究加重因素,r-HuEPO治疗采用不同剂量(125±70单位/千克/周)和方案(每周1.7±0.5次)——B组(表2)。两组的输血需求均消失,血细胞比容和血红蛋白显著升高(A组升高更明显)(表3)。铁蛋白水平显著下降(第12周时为147±30纳克/毫升 vs 27.5±11纳克/毫升)以及网织红细胞计数稳定(开始时为1.4% vs第12周时为2%)表明有铁消耗;与此同时,网织红细胞生成指数持续升高(开始时为1 vs第12周时为3)显示红细胞生成持续受到刺激(图1)。未观察到临床和/或血管并发症;动脉血压和血清钾水平未显著升高,因此在任何情况下均未取消r-HuEPO治疗。(摘要截选至250词)