Borawski J, Rydzewski A, Mazerska M, Kalinowski M, Pawlak K, Mysliwiec M
Department of Nephrology and Internal Medicine, Bialystok Medical School, Poland.
Nephrol Dial Transplant. 1996 Dec;11(12):2444-8. doi: 10.1093/oxfordjournals.ndt.a027212.
Amelioration of the anaemia of chronic renal failure and subsequent improved haemorheology result in correction of bleeding diathesis as evidenced by shortening of the skin bleeding time (BT). However, the relationship between the haematocrit and platelet-vessel wall interactions in haemodialysis (HD) patients under recombinant human erythropoietin (rHuEpo) therapy, assessed by platelet aggregation in response to ristocetin is more complex and somewhat inconsistent.
We investigated the relationship between haemoglobin (Hb) levels and whole blood ristocetin-induced platelet aggregation (electric impedance method) in 28 HD patients treated with rHuEpo, and with normal BT. The measurements were repeated in 16 subjects after having reduced platelet aggregability with orally administered ketanserin.
Ristocetin-induced platelet aggregation in the whole group was comparable to those found in 21 age-matched healthy subjects (normals) and in 25 HD patients not treated with rHuEpo (uraemics). Interestingly, a significant inverse correlation between this aggregation and Hb concentration was found (r = -0.392, P < 0.05). In the group of 16 patients, the pre-ketanserin aggregation was more intensive than in the normals and uraemics (P < 0.05). Ketanserin produced a fall in ristocetin-induced platelet aggregation (P < 0.02), prolongation of the BT (P < 0.02) and, unexpectedly, a decrease in serum Epo concentration (P < 0.0002) and the Hb level (P < 0.001). Again, an inverse correlation between depressed ristocetin-induced platelet aggregation and lowered Hb concentration was found (r = -0.590, P < 0.02). Moreover, a strong positive correlation between the extent of preketanserin platelet aggregation and the decrease in the intensity of this process that followed the trial was observed (r = 0.919, P < 0.000005). There were no changes in other haematological parameters or arterial blood pressure.
Considering the role of von Willebrand factor and fibrinogen in mediating ristocetin-induced platelet aggregation, and enhanced synthesis and/or release of these macromolecules in response to uraemia or inflammation, we suggest that exaggerated whole-blood platelet aggregability to ristocetin points to blunted erythropoiesis in HD patients on rHuEpo therapy.
慢性肾衰竭贫血的改善以及随之而来的血液流变学改善可纠正出血倾向，这可通过皮肤出血时间（BT）缩短得以证明。然而，在接受重组人促红细胞生成素（rHuEpo）治疗的血液透析（HD）患者中，通过对瑞斯托霉素的血小板聚集反应评估的血细胞比容与血小板 - 血管壁相互作用之间的关系更为复杂且有些不一致。
我们调查了28例接受rHuEpo治疗且BT正常的HD患者的血红蛋白（Hb）水平与全血瑞斯托霉素诱导的血小板聚集（电阻抗法）之间的关系。在16名受试者口服酮色林降低血小板聚集性后重复进行测量。
全组中瑞斯托霉素诱导的血小板聚集与21名年龄匹配的健康受试者（正常人）以及25名未接受rHuEpo治疗的HD患者（尿毒症患者）中的情况相当。有趣的是，发现这种聚集与Hb浓度之间存在显著负相关（r = -0.392，P < 0.05）。在16例患者组中，服用酮色林前的聚集比正常人和尿毒症患者更强烈（P < 0.05）。酮色林使瑞斯托霉素诱导的血小板聚集下降（P < 0.02），BT延长（P < 0.02），并且出乎意料的是，血清促红细胞生成素浓度下降（P < 0.0002）和Hb水平下降（P < 0.001）。再次发现，瑞斯托霉素诱导的血小板聚集降低与Hb浓度降低之间存在负相关（r = -0.590，P < 0.02）。此外，观察到服用酮色林前血小板聚集程度与试验后该过程强度降低之间存在强正相关（r = 0.919，P < 0.000005）。其他血液学参数或动脉血压没有变化。
考虑到血管性血友病因子和纤维蛋白原在介导瑞斯托霉素诱导的血小板聚集中的作用，以及这些大分子在尿毒症或炎症反应中合成和/或释放增加，我们认为接受rHuEpo治疗的HD患者对瑞斯托霉素的全血血小板聚集性过高表明红细胞生成不足。
