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<p>Pregnancy induces vascular, coagulation, and immune alterations that predispose to thrombotic microangiopathy (TMA). Within this spectrum—preeclampsia/ hemolysis, elevated liver enzymes, and low platelets syndrome (HELLP) and complement-mediated TMA (CM-TMA)—overlapping features complicate diagnosis, whereas management and prognosis diverge. A 39-year-old woman developed severe hypertension at 35&#xa0;weeks’ gestation, underwent emergency cesarean section for preeclampsia, and subsequently became anuric. She had schistocytic hemolysis, thrombocytopenia, elevated lactate dehydrogenase (LDH), and transaminitis. One plasma exchange, hemodialysis, and supportive care were provided; urine output recovered and dialysis ceased. Atypical complement tests results persisted for ~ 1&#xa0;month (undetectable serum CH50 with elevated C3/C4), with normal functional assays and no pathogenic variants in complement-regulatory genes. On subsequent testing with Ethylenediaminetetraacetic acid (EDTA) plasma, preserved at − 80&#xa0;°C, showed a normal CH50, suggesting that ex vivo complement activation may have contributed to the low serum CH50. In the acute setting,&#xa0;HELLP versus CM-TMA remained indeterminate, so management was guided by the clinical trajectory: brief plasma exchange during TTP evaluation, close monitoring, and deferral of complement inhibition as platelets, LDH, and urine output improved. This case supports a “trend-first” approach to peripartum TMA, and underscores ex vivo complement activation as a key pitfall when interpreting complement assays in the peripartum setting.</p>

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Postpartum TMA requiring dialysis with discordant complement tests: a case report

  • 期刊论文

  • 发表日期：

    2026年6月29日

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  • Hikari Fujimura,
  • Shun Minatoguchi,
  • Riku Takeuchi,
  • Ryosuke Umeda,
  • Yuka Sato,
  • Shigehisa Koide,
  • Asuka Horinouchi,
  • Noritoshi Kato,
  • Masashi Mizuno,
  • Hiroki Hayashi,
  • Midori Hasegawa,
  • Shoichi Maruyama,
  • Naotake Tsuboi

摘要

Pregnancy induces vascular, coagulation, and immune alterations that predispose to thrombotic microangiopathy (TMA). Within this spectrum—preeclampsia/ hemolysis, elevated liver enzymes, and low platelets syndrome (HELLP) and complement-mediated TMA (CM-TMA)—overlapping features complicate diagnosis, whereas management and prognosis diverge. A 39-year-old woman developed severe hypertension at 35 weeks’ gestation, underwent emergency cesarean section for preeclampsia, and subsequently became anuric. She had schistocytic hemolysis, thrombocytopenia, elevated lactate dehydrogenase (LDH), and transaminitis. One plasma exchange, hemodialysis, and supportive care were provided; urine output recovered and dialysis ceased. Atypical complement tests results persisted for ~ 1 month (undetectable serum CH50 with elevated C3/C4), with normal functional assays and no pathogenic variants in complement-regulatory genes. On subsequent testing with Ethylenediaminetetraacetic acid (EDTA) plasma, preserved at − 80 °C, showed a normal CH50, suggesting that ex vivo complement activation may have contributed to the low serum CH50. In the acute setting, HELLP versus CM-TMA remained indeterminate, so management was guided by the clinical trajectory: brief plasma exchange during TTP evaluation, close monitoring, and deferral of complement inhibition as platelets, LDH, and urine output improved. This case supports a “trend-first” approach to peripartum TMA, and underscores ex vivo complement activation as a key pitfall when interpreting complement assays in the peripartum setting.