Rare Case of Chronic Limb-Threatening Ischemia in a 32-Year-Old Patient with Nephrotic Syndrome: A Case Report

Author:

Afandy Jonathan Edbert1,Taofan Taofan2ORCID,Indriani Suci2,Batubara Edwin Adhi Darmawan1,Adiarto Suko2

Affiliation:

1. Assistant of Vascular Division, Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Indonesia, National Cardiovascular Center Harapan Kita, University of Indonesia Academic Hospital, Jakarta, Indonesia

2. Department of Cardiology and Vascular Medicine, Faculty of Medicine, University of Indonesia, National Cardiovascular Center Harapan Kita, University of Indonesia Academic Hospital, Jakarta, Indonesia

Abstract

AbstractChronic 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.

Publisher

Georg Thieme Verlag KG

Subject

Cardiology and Cardiovascular Medicine

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