背景:血栓性微血管病以微血管病性溶血性贫血为特征,血小板减少症,器官损伤。病理特征包括血管损伤,表现为小动脉和毛细血管血栓形成,内皮和血管壁有特征性异常。血小板减少是干扰素治疗的常见不良反应之一。然而,更严重但罕见的副作用是血栓性微血管病。
方法:我们报告一例36岁的亚洲男性患者,其临床表现为高血压,视力模糊,急性肾功能衰竭,血小板减少症,和血栓性微血管病.肾活检显示间质水肿伴纤维化,小动脉增厚伴玻璃体改变,和上皮足细胞节段性融合。免疫荧光显微镜显示C3(+),IgA(+)沉积在系膜区域,病理符合血栓性微血管病肾损伤和IgA沉积。患者有5年以上乙型肝炎病毒感染史。拉米夫定过去曾被使用过,但自2018年起使用长效干扰素联合富马酸替诺福韦艾拉酚胺注射液.综合临床调查和实验室检查诊断为干扰素引起的血栓性微血管病变。在他的治疗中停止干扰素后,患者的肾功能在3次治疗性血浆置换治疗和无免疫抑制剂的随访治疗后部分恢复.患者的肾功能保持稳定。
结论:本报告提示干扰素可诱发血栓性微血管病伴急性肾损伤,会发展成慢性肾功能不全.
BACKGROUND: Thrombotic microangiopathy is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ injury. The pathological features include vascular damage that is manifested by arteriolar and capillary thrombosis with characteristic abnormalities in the endothelium and vessel wall. Thrombocytopenia is one of the common adverse effects of
interferon therapy. However, a more serious but rare side effect is thrombotic microangiopathy.
METHODS: We report the
case of a 36-year-old Asian male patient with clinical manifestations of hypertension, blurred vision, acute renal failure, thrombocytopenia, and thrombotic microangiopathy. Renal biopsy showed interstitial edema with fibrosis, arteriolar thickening with vitreous changes, and epithelial podocytes segmental fusion. Immunofluorescence microscopy showed C3(+), Ig A(+) deposition in the mesangial region, which was pathologically consistent with thrombotic microangiopathy renal injury and Ig A deposition. The patient had a history of hepatitis B virus infection for more than 5 years. Lamivudine was used in the past, but the injection of long-acting
interferon combined with tenofovir alafenamide fumarate was used since 2018. The comprehensive clinical investigation and laboratory examination diagnosed the condition as thrombotic microangiopathy kidney injury caused by interferon. After stopping
interferon in his treatment, the patient\'s renal function partially recovered after three consecutive therapeutic plasma exchange treatments and follow-up treatment without immunosuppressant. The renal function of the patient remained stable.
CONCLUSIONS: This report indicates that
interferon can induce thrombotic microangiopathy with acute renal injury, which can progress to chronic renal insufficiency.