Ohzeki Mioko, Fukushima Tatsuo, Arakawa Sayaka, Ozeki Masahito, Kosaka Yoshihide, Kobayashi Shinya, Namikoshi Tamehachi, Haruna Yoshisuke, Sasaki Tamaki, Kashihara Naoki
Kawasaki Medical School, Department of Medicine, Division of Nephrology, Okayama, Japan.
Nihon Jinzo Gakkai Shi. 2005;47(7):834-8.
The present case was a 59-year-old woman who underwent a right nephrectomy at 30 years of age, and in whom renal dysfunction occurred at 51 years of age. In November 199X, when her creatinine level reached 7 mg/dl, renal replacement therapy was recommended. She refused this therapy and began her own diet therapy, which consisted of taking only supplement beverage, but no food. Afterwards she became unable to do daily work, and entered our hospital in July of the next year. On admission, her bleeding time was over 10 minutes, but coagulation function tests showed normal values. Platelet function tests showed that coagulation with the addition of ADP was mildly decreased and that coagulation with the addition of aggregation was severely decreased. These data and her bleeding tendency improved with hemodialysis. Therefore, a diagnosis of aggregation non-responsive uremic platelet dysfunction was made. On admission, we were not able to insert a catheter for hemodialysis because of her severe bleeding tendency. A platelet transfusion was made so that we could insert the catheter without severe bleeding. However, this hemostatic effect lapsed after about five to six hours. Six hours after insertion of the catheter, oozing from the orifice of the catheter was seen and a red blood transfusion was necessary. Three days after beginning hemodialysis, the bleeding tendency was no longer seen. Her platelet function and coagulation test results also improved. We can make two conclusions regarding this case. The first is when the physician's medical strategy cannot be carried out due to uremic platelet dysfunction, a platelet transfusion can temporarily eliminate the bleeding tendency. The second is that the pathophysiology of uremic platelet dysfunction involves suppression of the primary step of platelet aggregation with collagen. Experience with the present case revealed the appropriate therapeutic strategy for the pathophysiology of uremic platelet dysfunction.
本病例为一名59岁女性，30岁时接受了右肾切除术，51岁时出现肾功能障碍。199X年11月，当她的肌酐水平达到7mg/dl时，建议进行肾脏替代治疗。她拒绝了这种治疗，开始自行饮食疗法，即只饮用补充饮料，不进食。此后，她无法进行日常工作，于次年7月入住我院。入院时，她的出血时间超过10分钟，但凝血功能检查显示正常。血小板功能检查显示，添加ADP后的凝血轻度降低，添加聚集剂后的凝血严重降低。这些数据以及她的出血倾向通过血液透析得到改善。因此，诊断为聚集无反应性尿毒症血小板功能障碍。入院时，由于她严重的出血倾向，我们无法插入血液透析导管。进行了血小板输注，以便我们能够在无严重出血的情况下插入导管。然而，这种止血效果在大约五到六个小时后消失。插入导管六小时后，可见导管口渗血，需要输注红细胞。开始血液透析三天后，出血倾向不再出现。她的血小板功能和凝血检查结果也有所改善。关于这个病例我们可以得出两个结论。第一个结论是，当由于尿毒症血小板功能障碍而无法实施医生的治疗策略时，血小板输注可以暂时消除出血倾向。第二个结论是，尿毒症血小板功能障碍的病理生理学涉及胶原蛋白对血小板聚集初级步骤的抑制。本病例的经验揭示了针对尿毒症血小板功能障碍病理生理学的适当治疗策略。
