Anti-glomerular basement membrane antibody disease complicated by posterior reversible encephalopathy syndrome
Anti-glomerular basement membrane antibody disease complicated by posterior reversible encephalopathy syndrome
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DOI：
10.1080/24725625.2020.1816640
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发表时间：
2021-01-02
影响因子：
0.8
通讯作者：
Hanaoka，Ryosuke
中科院分区：
文献类型：
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作者：
Taniguchi，Yumeko;Hanaoka，Ryosuke
抗肾小球基底膜（抗GBM）抗体疾病是一种罕见的小血管炎。可逆性后部脑病综合征（PRES）是一种基于相似的神经影像学表现将异质性病因组合在一起的综合征。我们报告了一个罕见的情况下，谁接受治疗的抗GBM抗体疾病谁开发的PRES。一个33岁的妇女提出了严重的全身水肿，蛋白尿，血尿和cylindruria。基于抗GBM抗体和尿分析的阳性结果，她被诊断患有抗GBM抗体疾病。最终需要血液透析。患者接受类固醇治疗、血浆置换治疗和静脉注射环磷酰胺，沿着红细胞输注治疗进行性贫血。输血后，患者出现恶心、严重头痛、幻视和躁动，随后出现癫痫发作和血压迅速升高。影像学检查诊断为PRES。随着抗GBM抗体的降低，肾功能衰竭得到改善，血液透析停止。给予苯妥英，癫痫消失。虽然我们不能排除该患者因抗GBM抗体疾病接受的治疗导致PRES发生的可能性，但我们推测导致PRES发生的内皮功能障碍不仅是由已知的风险因素（如细胞毒性药物、输血或肾衰竭）引起的，还可能是由抗GBM抗体疾病引起的免疫异常和随后的炎症反应引起的。这些因素可能是PRES和抗GBM抗体病共同的病理生理机制。
Anti-glomerular basement membrane (anti-GBM) antibody disease is a rare type of small-vessel vasculitis. Posterior reversible encephalopathy syndrome (PRES) is a syndrome of heterogeneous aetiologies grouped together based on similar neuroimaging findings. We report a rare case of a patient who received treatment for anti-GBM antibody disease who developed PRES. A 33-year-old woman presented with severe generalised oedema, proteinuria, haematuria, and cylindruria. She was diagnosed with anti-GBM antibody disease based on positive findings for anti-GBM antibodies and urinalysis. Haemodialysis was eventually required. She received steroid therapy, plasma exchange therapy, and intravenous cyclophosphamide, along with a red blood cell transfusion for progressive anaemia. After the transfusion, she experienced nausea, severe headache, visual hallucinations, and agitation followed by seizures and a rapid increase in blood pressure. Imaging studies led to a diagnosis of PRES. Renal failure improved with the decrease in anti-GBM antibodies, and haemodialysis was discontinued. Phenytoin was administered, and seizures disappeared. Although we cannot rule out the possibility that the treatment this patient underwent for anti-GBM antibody disease led to the development of PRES, we speculate that endothelial dysfunction leading to the development of PRES is caused not only by known risk factors such as cytotoxic agents, blood transfusions, or renal failure, but also by immunological abnormalities and subsequent inflammatory reactions due to anti-GBM antibody disease. These factors may be shared pathophysiologic mechanisms of PRES and anti-GBM antibody disease.