32岁肾病综合征患者发生罕见的慢性危及肢体缺血1例

IF 0.5 Q4 PERIPHERAL VASCULAR DISEASE
Jonathan Edbert Afandy, Taofan Taofan, Suci Indriani, Edwin Adhi Darmawan Batubara, Suko Adiarto
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引用次数: 0

摘要

慢性肢体威胁缺血是外周动脉疾病(PAD)的终末阶段,主要影响60岁以上的个体。虽然相当罕见,但肾病综合征(NS)被认为会增加动脉血栓栓塞(ATE)的易感性。A某(32岁)称左腿静息性疼痛,右腿步行50米后感到疼痛。患者有9年活检证实的NS病史,每日给药2 × 360 mg霉酚酸和1 × 8 mg甲基强的松龙。无高血压、糖尿病、吸烟史。左腿出现萎缩和溃疡。实验室检查显示d -二聚体升高,胆固醇水平接近高水平。右踝肱指数为0.5,左踝肱指数为0.33。计算机断层血管造影发现左髂外动脉和右股浅动脉(SFA)闭塞。患者接受了经皮腔内血管成形术,在双腿上放置了一个普通球囊,并在左侧SFA上放置了一个额外的药物洗脱支架。出院时使用利伐沙班、氯吡格雷、阿司匹林、辛伐他汀、霉酚酸和甲基强的松龙,无任何症状。ns引起ATE的机制尚不清楚,尽管它与尿液中抗凝血剂的丧失、促凝活性的增加、纤维蛋白溶解系统的改变、血小板增多和血小板活化增强有关。在NS管理中,长期的皮质类固醇治疗也会通过促进高凝状态而增加血栓栓塞的风险。我们怀疑NS和长期使用皮质类固醇是ATE的危险因素,在我们的患者中表现为PAD。虽然最佳NS治疗可降低PAD的风险,但应密切监测长期使用皮质类固醇。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Rare Case of Chronic Limb-Threatening Ischemia in a 32-Year-Old Patient with Nephrotic Syndrome: A Case Report
Abstract Chronic limb-threatening ischemia represents the end stage of peripheral artery disease (PAD), primarily affecting individuals over 60 years old. While quite rare, nephrotic syndrome (NS) is recognized for increasing the susceptibility to arterial thromboembolism (ATE). A 32-year-old male complained of resting pain in his left leg and pain after walking 50 meters with his right leg. He had a 9-year history of NS confirmed through biopsy and was on a daily regimen of 2 × 360 mg mycophenolic acid and 1 × 8 mg methylprednisolone. He had no history of hypertension, diabetes, or smoking. Atrophy and ulcers were observed on his left leg. Laboratory tests revealed elevated D-dimer and borderline high cholesterol levels. The right ankle-brachial index was 0.5, and for the left, it was 0.33. Computed tomography angiography identified occlusion in the left external iliac artery and right superficial femoral artery (SFA). The patient underwent percutaneous transluminal angioplasty with a plain balloon on both legs and an additional drug-eluting stent on the left SFA. He was discharged on rivaroxaban, clopidogrel, aspirin, simvastatin, mycophenolic acid, and methylprednisolone, with no complaints. The mechanism behind NS-caused ATE remains unclear, although it is associated with the loss of anticoagulants in urine, increased procoagulant activity, altered fibrinolytic systems, thrombocytosis, and enhanced platelet activation. Prolonged corticosteroid therapy in NS management also amplifies the risk of thromboembolism by promoting a hypercoagulable state. We suspected NS and the prolonged use of corticosteroids as risk factors for ATE, manifested as PAD in our patient. While optimal NS therapy may reduce the risk of PAD, prolonged corticosteroid use should be closely monitored.
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来源期刊
International Journal of Angiology
International Journal of Angiology PERIPHERAL VASCULAR DISEASE-
CiteScore
1.30
自引率
16.70%
发文量
57
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