Thrombotic microangiopathy (TMA) is an emerging complication of oncologic therapy. Cancer-related causes of renal endothelial cell damage include cytotoxic chemotherapies, radiation given for myeloablation, and direct involvement of renal vasculature by tumor cells. Another class of therapeutic agents that has been implicated in TMA is the vascular endothelial growth factor (VEGF) pathway inhibitors, including the anti-VEGF monoclonal antibody bevacizumab and the VEGF receptor tyrosine kinase inhibitor sunitinib. These TMAs have been termed type II cancer drug-induced TMA and are distinguished from those associated with some cytotoxic chemotherapies (ie, type I) in that they are not dose dependent and patients are more likely to demonstrate some recovery of kidney function. Determination of the cause of TMA in oncologic patients often presents a significant challenge because patients frequently receive multiple chemotherapeutic agents simultaneously and clinicopathologic features often demonstrate substantial overlap, regardless of cause. We present a case of TMA with predominantly chronic features in a 70-year-old patient being treated for adenoid cystic carcinoma of the breast with a single agent, a short interfering RNA targeted against Myc (DCR-MYC).

中文翻译：

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由于DCR-MYC（一种Myc靶向的短干扰RNA）导致的慢性微血管病。

血栓性微血管病（TMA）是一种新兴的肿瘤治疗并发症。肾内皮细胞损害的与癌症相关的原因包括细胞毒性化学疗法，给予骨髓消融的放射线以及肿瘤细胞直接参与肾血管的作用。与TMA有关的另一类治疗剂是血管内皮生长因子（VEGF）途径抑制剂，包括抗VEGF单克隆抗体贝伐单抗和VEGF受体酪氨酸激酶抑制剂舒尼替尼。这些TMA被称为II型癌症药物诱导的TMA，与那些与某些细胞毒性化学疗法（即I型）相关的TMA区别在于它们不是剂量依赖性的，患者更有可能表现出肾脏功能的某些恢复。肿瘤患者中TMA病因的确定通常面临重大挑战，因为无论原因如何，患者经常同时接受多种化疗药物，而且临床病理特征经常表现出实质性的重叠。我们介绍了一个在70岁的患者中以主要慢性特征为特征的TMA病例，该患者正在接受单药，针对Myc的短干扰RNA（DCR-MYC）治疗乳腺癌的腺样囊性癌。