肾移植后红细胞增多症，对血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂难治。
Post-transplant erythrocytosis refractory to ACE inhibitors and angiotensin receptor blockers.
作者信息
Vishnu Prakash, Moreno Vanegas Yenny, Wadei Hani M, Rivera Candido E
机构信息
Department of Hematology and Oncology, Mayo Clinic, Florida, US.
Department of Transplant Nephrology, Mayo Clinic, Florida, US.
出版信息
BMJ Case Rep. 2018 Jun 28;2018:bcr-2018-224622. doi: 10.1136/bcr-2018-224622.
Post-transplant erythrocytosis (PTE) is a condition with elevated haematocrit (hct) in renal allograft recipients. The mainstay of treatment is ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARB), but seldom phlebotomy. PTE must be recognised early to prevent major thromboembolic events. We present a case of PTE that was refractory to blockade of renin-angiotensin system (RAS) by ACEi and ARB and required phlebotomy for control of hct. Our review of medical literature about prevalence and pathophysiology of PTE suggests that approximately 22% of patients with PTE are refractory to ACEi/ARB treatment. There are four plausible pathways that appear to play a role in causing PTE: disruption of erythropoietin regulation, mitogenic effect of the RAS on erythroid lineage, insulin-like growth factor 1 and androgenic stimulation. Presently, there is no unifying hypothesis involving these factors, but refractoriness to ACEi/ARB may represent a distinct subcategory of PTE.
移植后红细胞增多症（PTE）是肾移植受者中出现血细胞比容（hct）升高的一种病症。治疗的主要方法是使用血管紧张素转换酶抑制剂（ACEi）或血管紧张素II受体阻滞剂（ARB），但很少进行放血治疗。必须尽早识别PTE以预防重大血栓栓塞事件。我们报告一例PTE病例，该病例对ACEi和ARB阻断肾素-血管紧张素系统（RAS）无效，需要进行放血治疗以控制hct。我们对有关PTE患病率和病理生理学的医学文献进行的综述表明，约22%的PTE患者对ACEi/ARB治疗无效。有四条看似在导致PTE中起作用的合理途径：促红细胞生成素调节的破坏、RAS对红系谱系的促有丝分裂作用、胰岛素样生长因子1和雄激素刺激。目前，尚无涉及这些因素的统一假说，但对ACEi/ARB难治可能代表PTE的一个独特亚类。
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