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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Catastrophic Antiphospholipid Syndrome (CAPS) is a rare,life-threatening variant of Antiphospholipid Syndrome (APS)characterized by rapid, multi-organ thrombosis. Its presentation is often complex, mimicking other systemic diseases. We present a case of a young female who initially presented with features of rapidly progressive renal failure and decompensated liver disease and subsequently developed systemic collapse, ultimately diagnosed as CAPS with renal thrombotic microangiopathy and hepatic budd chiari syndrome
The patient was a 19-year-old female who came with a one month history of occasional fever and jaundice, followed by distension of abdomen and swelling of feet for last 2 weeks. She did not have other systemic complaints , had never been pregnant and denied recent intake of any medications or drugs .On examination,she was found to be hypertensive with anasarca,anemia and jaundice.Initial investigations included basic blood tests, tropical fever profile, and urine analysis which revealed hepatic and renal dysfunction which was rapidly progressive(peak serum creatinine 9.8mg/dl)along with anemia, thrombocytopenia and subnephrotic Proteinuria.
A renal biopsy was done after two sessions of hemodialysis along with imaging studies such as USG Whole Abdomen with Splenoportal axis Doppler,Hepatic Venogram and an upper GI Endoscopy to evaluate liver disease.
Autoimmune workup and a liver biopsy were also performed subsequently.
Renal biopsy showed thrombotic microangiopathy (TMA) with an IFTA of 30%.
Other evaluation revealed decompensated cirrhosis with portal hypertension. Imaging confirmed stenosed hepatic veins, extensive veno-venous collaterals, and a near-complete occlusion of the intrahepatic and suprahepatic IVC, leading to a diagnosis of primary Budd-Chiari Syndrome (BCS). She underwent an IVC plasty and was treated with diuretics and anticoagulants. Her renal function improved partially and she maintained a serum creatinine 3mg/dl without hemodialysis.The immunological workup was significant for a positive Lupus Anticoagulant and ASMA but other markers like ANA,ANA Profile were negative. Despite an initial IVC plasty, the patient's condition rapidly worsened with coagulopathy,persistent hypotension, and evidence of new thromboses including in the left popliteal vein and a non-opacified hepatic vein on Doppler USG. This constellation of multi-organ thrombosis in the setting of positive antiphospholipid antibodies suggested the diagnosis of probable Catastrophic APLA Syndrome. She received glucocorticoids and underwent 2 sessions of plasma exchange but subsequently developed sepsis and was on mechanical ventilation before succumbing.
This case illustrates a rare and severe presentation of Catastrophic APS manifesting clinically as rapidly worsening renal and hepatic dysfunction and pathologically as Renal thrombotic microangiopathy and hepatic Budd-chiari syndrome. The rapid deterioration ending in mortality despite intervention underscores the aggressive nature of CAPS. An early,accurate etiological diagnosis is crucial for improving survival chances in such complex cases involving systemic autoimmune disorders. The usual classification criteria of APS may not always be clinically apparent.
