马兜铃酸肾病继发视神经损害一例临床分析  

Clinical analysis of aristolochic acid nephropathy with optic atrophy

作　　者：王惠娟[1] 赵玲 高阳[3] 

机构地区：[1]河北医科大学第二医院神经内科,石家庄050000 [2]鹿泉市人民医院内科 [3]石家庄市第一人民医院神经内科

出　　处：《脑与神经疾病杂志》2009年第4期307-309,共3页Journal of Brain and Nervous Diseases

摘　　要：目的探讨马兜铃酸肾病视力损害。方法分析1例以视神经损害住神经科而后经检查诊断为马兜铃酸肾病。患者的临床表现为突然进行性双眼视力障碍,病前有恶心、呕吐病史2月,有服用"龙胆泻肝丸"3～4年史。查体贫血貌,双眼底视乳头边界不清,色苍白,两瞳孔直接、间接对光反射消失。检测显示中度贫血、低血钾、代谢性酸中毒、肾性糖尿、肾功能衰竭。腰椎穿刺脑脊液压力正常。结果依据病史、查体、临床检测诊断为马兜铃酸肾病继发视神经损害。结论马兜铃酸肾病可继发视神经损害。Objective To explore the optic impair in the patients with aristolochic acid nephropathy. Methods Analysis a case who was admitted to department of neurology suffering from sudden blindness of two eyes, and at last she was diagnosed as Aristolochic acid nepbropathy. This patient had taken in chinese traditional medicine which contain aristolochic acid for 3 or 4 years. She had anorexia and vomited for 2 months with no weight loss. 4 days before she was admitted to hospital, she suddenly suffered blindness of two eyes. Physical examination ： Anemia Maung. Bilateral papilledema and optic disk pallor. The pupils were equal in size with no the direct and indirectillumination response. Test results： RBC （2.44 x 101Z/L, normal level 3.50-5.50 x 1012/L）, Hemoglobin（Hgb） （79g/L, normal level 110 - 160 g/L） and serum kalium （2.92retool/L, normal level 3.5 - 5.5 mmol/L） were all decreased. Serum urea nitrogen （22.30mmoL/L, normal level 1.7 -7.1 mmol/L）, Creatinine （519.30ummol/L, normal level 0.1 - 136 ummol/L） and metabolic acidosis were elevated. Renal function was failed. Routine urine analysis showed： glucose （ ＋ ） but blood sugar was normal. CSF pressure was normal （101mmH20, normal level 80 - 180 mmH2O）. Results Approach to diagnosis： Aristolochic acid nephropathy with optic impair. Conclusion Optic impair can occur in aristolochic acid nephropathy.

关 键 词：马兜铃酸 马兜铃酸肾病 视神经损害 

分 类 号：R595[医药卫生—内科学]