Budd–Chiari Syndrome in the Background of Chronic Kidney Disease: A Hypercoagulability‐Driven Association or Coincidence? A Case Report

Budd-Chiari syndrome (BCS) is a rare condition characterized by hepatic venous outflow obstruction and is often associated with thrombosis or fibrous membranes (webs). To our knowledge, this is the first reported case of BCS occurring secondary to chronic kidney disease (CKD). This case emphasizes the complex reno-vascular-hepatic interplay and expands current literature. A 48-year-old female with stage V CKD on hemodialysis presented with signs of portal hypertension. Imaging revealed an IVC web causing BCS. Procoagulant workup showed elevated fibrinogen, PAI-1, and homocysteine, suggesting CKD-induced thrombosis as a possible trigger. She was managed with anticoagulation (enoxaparin, warfarin), diuretics, and beta-blockers. Her symptoms stabilized, explaining BCS as a hypercoagulability-driven complication rather than a coincidence. CKD creates a prothrombotic state through impaired fibrinolysis, endothelial and platelet dysfunction, and elevated procoagulants, potentially contributing to BCS. Though inherited or acquired thrombophilias are common causes of BCS, CKD-related hypercoagulability may also play a significant role. Diagnosis relies on Doppler ultrasound and confirmatory CT or magnetic resonance imaging (MRI). Management ranges from anticoagulation to endovascular or surgical interventions. This case illustrates a rare overlap, where CKD may have triggered IVC web formation causing venous obstruction, emphasizing the need to consider thrombosis risk in CKD patients with unexplained signs of liver dysfunction to prevent cirrhosis. BCS should be suspected in patients on chronic hemodialysis presenting with unexplained ascites, hepatosplenomegaly, and abdominal pain. Timely imaging, hypercoagulability assessment, and individualized therapy are essential for optimal outcomes in this rare but critical complication of CKD.