Rigotti P, Flechner S M, Van Buren C T, Payne W T, Kahan B D
Int Surg. 1986 Jan-Mar;71(1):38-41.
Six of 325 patients undergoing renal transplantation under combined cyclosporine (CsA)-prednisone immunosuppression displayed renal artery thrombosis between 4 and 12 days after transplantation. All six patients had satisfactory initial revascularization, as ascertained by radionuclide scan and renal function. In none was the thrombosis considered to be secondary to rejection, either by clinical course or upon renal biopsy. Since there was no clear etiologic factor and since none of the overlapping 297 patients treated with azathioprine-prednisone displayed this complication, these cases appear to support the hypothesis that CsA alters intravascular hemostatic homeostasis. Data in experimental models are consistent with a predisposing factor to thrombosis, namely CsA reduces the synthesis of prostacyclin stimulating factors, leading to decreased prostacyclin production by vascular endothelial cells, and to failure to inhibit platelet aggregation.
在接受环孢素(CsA)-泼尼松联合免疫抑制的325例肾移植患者中,有6例在移植后4至12天出现肾动脉血栓形成。通过放射性核素扫描和肾功能检查确定,所有6例患者最初的血管再通情况良好。无论是从临床病程还是肾活检来看,均未认为血栓形成是由排斥反应继发所致。由于没有明确的病因,且在接受硫唑嘌呤-泼尼松治疗的297例重叠患者中均未出现这种并发症,这些病例似乎支持了CsA改变血管内止血稳态的假说。实验模型中的数据与血栓形成的一个易感因素一致,即CsA减少前列环素刺激因子的合成,导致血管内皮细胞产生的前列环素减少,并且无法抑制血小板聚集。