Okawa Hiroyuki, Wada Yukihiro, Takeuchi Kazuhiro, Motohashi Tomomi, Abe Tetsuya, Uchitsubo Ryota, Kawamura Naohiro, Kawamura Sayumi, Sakurabayashi Shun, Honda Kosuke, Morishita Masamitsu, Naito Shokichi, Aoyama Togo, Takeuchi Yasuo
Department of Nephrology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa, 252-0375, Japan.
Department of Nephrology, Morishita Memorial Hospital, Sagamihara, Japan.
CEN Case Rep. 2025 Jun;14(3):442-449. doi: 10.1007/s13730-025-00978-3. Epub 2025 Mar 3.
Both thrombotic thrombocytopenic purpura (TTP) and malignant hypertension (MHT) present with thrombotic microangiopathy (TMA). Combination therapy with caplacizumab, anti-von Willebrand factor (VWF) A1 domain antibody, and plasma exchange (PE) has recently been highlighted as a novel therapeutic option for TTP. We treated a 51-year-old woman who showed severe hypertension, retinopathy, and acute kidney injury. Level of consciousness was clear on admission, but low-grade fever was observed. Laboratory tests showed normocytic anemia, thrombocytopenia, renal dysfunction, and a slight decrease in haptoglobin. Neither disseminated intravascular coagulation nor leukemia was diagnosed. The patient emergently received intravenous antihypertensive therapy, continuous hemodiafiltration, and sufficient blood transfusion. However, thrombocytopenia and oliguria remained despite control of blood pressure. On hospital day 8, administration of caplacizumab combined with PE was initiated before receiving results for a disintegrin-like and metalloprotease with thrombospondin type 1 motifs 13 (ADAMTS13) activity and inhibitor levels. We then administered caplacizumab for 5 days and performed 2 sessions of PE until confirming ADAMTS13 activity of 42% and absence of its inhibitor, contributing to increased serum hemoglobin and platelet levels with cessation of dialysis. Renal biopsy findings on hospital day 20 showed arteriolar nephrosclerosis and intimal hyperplasia in small arteries. To the best of our knowledge, this represents the first description of MHT-induced TMA treated with caplacizumab. MHT-induced TMA exhibiting symptoms of TTP tends to show poor renal prognosis, so early administration of caplacizumab with PE before receiving results for ADAMTS13 might prove beneficial for cases in which MHT complicated with TTP is suspected.
血栓性血小板减少性紫癜(TTP)和恶性高血压(MHT)均表现为血栓性微血管病(TMA)。最近,卡泊单抗(一种抗血管性血友病因子(VWF)A1结构域抗体)与血浆置换(PE)的联合治疗已成为TTP的一种新型治疗选择。我们治疗了一名51岁的女性,她表现出严重高血压、视网膜病变和急性肾损伤。入院时意识清醒,但观察到低热。实验室检查显示正细胞性贫血、血小板减少、肾功能不全,触珠蛋白略有下降。未诊断出弥散性血管内凝血和白血病。患者紧急接受静脉降压治疗、持续血液透析滤过和充足的输血。然而,尽管血压得到控制,但血小板减少和少尿仍然存在。在住院第8天,在获得具有血小板反应蛋白基序的解整合素样金属蛋白酶13(ADAMTS13)活性和抑制剂水平的结果之前,开始给予卡泊单抗联合PE治疗。然后我们给予卡泊单抗5天,并进行了2次PE治疗,直到确认ADAMTS13活性为42%且无其抑制剂,这使得血清血红蛋白和血小板水平升高,透析停止。住院第20天的肾活检结果显示小动脉性肾硬化和小动脉内膜增生。据我们所知,这是首次描述用卡泊单抗治疗MHT诱导的TMA。表现出TTP症状的MHT诱导的TMA往往显示出较差的肾脏预后,因此在获得ADAMTS13结果之前早期给予卡泊单抗联合PE可能对怀疑MHT合并TTP的病例有益。