Abstract: FR-PO0993
Complement in Crisis: Pregnancy-Triggered Atypical Hemolytic Uremic Syndrome
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
- Khurana, Shriya, MedStar Washington Hospital Center, Washington, District of Columbia, United States
- Thach, Lonnie, MedStar Washington Hospital Center, Washington, District of Columbia, United States
Introduction
Pregnancy-associated thrombotic microangiopathy (TMA) is a rare but life-threatening condition. Distinguishing thrombotic thrombocytopenic purpura (TTP) from complement-mediated TMA (atypical hemolytic uremic syndrome, aHUS) is critical, as management differs significantly and delays may worsen renal outcomes.
Case Description
34-year-old G2P1001 woman with recent spontaneous miscarriage presented with abdominal pain, nausea, vomiting, and vaginal spotting. On presentation, she was tachycardic and oliguric (60 mL/12 hours). Evaluation revealed leukocytosis (23K), anemia (Hgb 6.1 g/dL), thrombocytopenia (Plt 45K), LDH ~2000, and acute kidney injury (creatinine 12.6 mg/dL from baseline 0.8). Urinalysis showed hematuria (>182 RBCs/hpf). Peripheral smear demonstrated schistocytes, consistent with microangiopathic hemolysis.
Given concern for pregnancy-associated TMA, she was admitted to the ICU and empirically treated for TTP with plasma exchange (PLEX) and corticosteroids. She completed 7 PLEX sessions and required hemodialysis. Platelets normalized, but renal failure persisted.
ADAMTS13 activity was 67% (repeat 59%), making TTP unlikely and favoring aHUS, though complement genetic testing was negative. Kidney biopsy confirmed thrombotic microangiopathy with acute tubular injury (image). She was treated with eculizumab, after which urine output increased and creatinine improved to 3.08 mg/dL, then further to 2.7 mg/dL, allowing dialysis discontinuation prior to discharge.
Discussion
This case highlights a high-stakes diagnostic dilemma in pregnancy-associated TMA. Initial presentation raised concern for TTP, warranting urgent empiric PLEX given the high mortality if untreated. However, preserved ADAMTS13 activity shifted the diagnosis toward aHUS. Pregnancy is a potent trigger for complement dysregulation, and negative genetic testing does not exclude aHUS, which remains primarily a clinical diagnosis. Kidney biopsy was critical in confirming TMA and guiding therapy. While PLEX remains first-line for suspected TTP, terminal complement inhibition is essential in aHUS, enabling renal recovery even after dialysis-dependent AKI.
Renal Biopsy