Abstract: FR-PO0991
When Treatment Precedes Diagnosis: Thrombotic Thrombocytopenic Purpura (TTP) vs. Complement-Mediated Thrombotic Microangiopathy (c-TMA)
Session Information
- Women's Health and Kidney Diseases
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Women's Health and Kidney Diseases
- 2100 Women's Health and Kidney Diseases
Authors
- Ozair, Saleha, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
- Block, Clay A., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
- Plessias, Charalampos, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
- Rajan, Roy, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
- Kaneko, Thomas M., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
Introduction
Pregnancy-associated TMA presents with overlapping features of TTP, HELLP, and c-TMA, often necessitating empiric therapy before a definitive diagnosis can be made.
Case Description
A 33-year-old female with Bipolar disorder, Hashimoto’s thyroiditis, Raynaud’s phenomenon presented at 33 weeks gestation with severe preeclampsia complicated by placental abruption, and hepatic infarction requiring emergent cesarean section. Postoperatively, she developed oligoanuric acute kidney injury (AKI) with metabolic acidosis. Labs revealed serum sodium 125 mmol/L, bicarbonate 14 mmol/L, creatinine 3.93 mg/dL, AST 1485 U/L, ALT 332 U/L, platelets 28000, hemoglobin 7.4 g/dL, LDH >2500 U/L, undetectable haptoglobin, D-dimer 19,000 ng/mL, and coagulopathy, consistent with microangiopathic hemolytic anemia (MAHA). PLASMIC score was 6.
Plasma exchange (PLEX) was initiated empirically while awaiting ADAMTS13 activity, and continuous renal replacement therapy was started for worsening acidosis. ADAMTS13 activity returned at 39%, after which PLEX was discontinued, as this level was felt to be too high to be explained by 1–2 units of plasma given before PLEX initiation. Complement studies were unfortunately not obtained prior to PLEX. Given persistent concern for c-TMA, therapy was transitioned to eculizumab following vaccination and antimicrobial prophylaxis. She completed 12 weeks of therapy and transitioned to intermittent hemodialysis.
Renal biopsy was deferred due to ongoing thrombocytopenia and coagulopathy. Urine microscopy showed renal tubular epithelial cells and dysmorphic red blood cells. Genetic testing revealed an ANLN variant associated with autosomal dominant focal segmental glomerulosclerosis (FSGS).
Discussion
This case highlights the need to obtain complement studies prior to plasma exchange whenever feasible to preserve diagnostic clarity. With the placenta acting as a potential complement regulatory “sink”, removal of it may have unmasked postpartum TMA. A previously uncertain ANLN variant, now reclassified as pathogenic for autosomal dominant FSGS, may have contributed to podocyte vulnerability through podocyte-endothelial crosstalk within the filtration barrier [1,2]. As our understanding of these pathways evolves, genetic and mechanistic insights may help identify specific groups or pathways that could be targeted by future pharmacologic therapies.