Abstract: FR-PO0933
Renal Thrombotic Microangiopathy as the Primary Manifestation of Heparin-Induced Thrombocytopenia: A Diagnostic and Therapeutic Challenge
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Shakaib, Mohammed I., Ascension Illinois, Chicago, Illinois, United States
- Dutta, Ujjwal, GMERS Medical College Gotri Vadodara, Vadodara, GJ, India
- Rajamani, Gurudharshan, Madras Medical College and Government General Hospital, Chennai, TN, India
- Keluskar, Harshada Santosh, Kazanskij gosudarstvennyj medicinskij universitet Ministerstva zdravoohranenia Rossijskoj Federacii, Kazan, Tatarstan, Russian Federation
- Shakaib, Yusuf M, Northwestern University, Evanston, Illinois, United States
- Bhatt, Jugal Hiren, GMERS Medical College Gotri Vadodara, Vadodara, GJ, India
Introduction
Heparin-induced thrombocytopenia (HIT) typically causes thrombocytopenia and thrombosis but can infrequently present as renal thrombotic microangiopathy (TMA), mimicking primary TMA syndromes like TTP or atypical hemolytic uremic syndrome (aHUS). Differentiation is essential, as management strategies diverge significantly. While HIT is classically associated with thrombocytopenia and thrombosis, it can infrequently manifest as TMA, mimicking primary TMA syndromes such as TTP or aHUS.
Case Description
An 81F with severe AS underwent TAVR. On day 14, she developed AKI (Cr 6.8), thrombocytopenia (34×10^9/L), low haptoglobin, but no schistocytes. ADAMTS13 was 79%. HIT was confirmed (PF4 antibodies, positive serotonin release assay). Argatroban failed to prevent new femoral DVT. Renal biopsy showed TMA: endothelial swelling, fibrin thrombi, RBC fragmentation, mesangiolysis, RBC casts, no complement/immune deposits. No vasculitis or atheroembolism. Anticoagulation was switched to bivalirudin. Plasma exchange/complement inhibition were deferred.
Discussion
This case shows a rare HIT-associated renal TMA that mimicked primary TMAs but lacked hemolysis markers. Normal ADAMTS13 & absence of schistocytes created diagnostic uncertainty, highlighting biopsy’s role in defining AKI etiology in prothrombotic states. Early HIT recognition & biopsy-guided exclusion of mimics were key to avoiding unnecessary plasma exchange. Biopsy confirmed TMA without complement/TTP features, ruled out atheroemboli/vasculitis, and guided treatment. Delayed HIT post-TAVR stresses nephrologist vigilance. Argatroban failure suggests HIT-TMA may need more aggressive anticoagulation. This case redefines HIT’s renal spectrum & biopsy’s diagnostic role.
Glomerulus with features of acute TMA including endothelial swelling, RBC fragmentation, karyorrhexis