Abstract: FR-PO031
Atypical Abruptio Placentae with AKI: Interventional Dilemma
Session Information
- AKI: Epidemiology, Risk Factors, and Prevention - 2
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Baloch, Muhammad Yasir, Washington University in St Louis, St Louis, Missouri, United States
- Portales Castillo, Ignacio A., Washington University in St Louis, St Louis, Missouri, United States
- Humphreys, Benjamin D., Washington University in St Louis, St Louis, Missouri, United States
Introduction
Alterations in the complement cascade can affect many organs and lead to renal, hematological, or obstetric complications. Here, we present a case of pregnancy complicated by abruptio placentae and severe acute kidney injury (AKI) requiring dialysis, where we identified a genetic predisposition to complement dysregulation.
Case Description
A 37-year-old female G5P3 at 36 weeks pregnancy, presented to the ER with abdominal pain. Fetal bradycardia was detected, prompting an urgent C-section. During surgery, placental abruption was diagnosed, she became hypotensive, requiring 2 liters of blood products. Post-surgery, she was anuric despite intravenous fluids and resolution of hypotension. Laboratory results were notable for AKI (Cr 2.2), transaminitis, anemia (Hb 7.6), thrombocytopenia (Plt 80), low haptoglobin, fibrinogen of 422md/dl and very elevated lactate dehydrogenase (LDH) at 3080U/L. The peripheral blood smear showed few schistocytes. Complement levels and ADAMTS13 were unremarkable. Hemodialysis was initiated on day 2. The clinical diagnosis was thrombotic microangiopathy (TMA) secondary to either HELLP syndrome vs atypical hemolytic uremic syndrome (aHUS). Eculizumab was considered but not given as her hematologic parameters rapidly improved. Two weeks later, she remained dialysis dependent. Three weeks after admission results of genetic testing for complement pathway related genes, revealed homozygous bi-allelic loss of Complement Factor H (CFHR3 – CFHR1) genes, which has been recently categorized as pathogenic. Eculizumab was then started. Her renal function improved, and she successfully transitioned off dialysis.
Discussion
Despite carrying pathogenic variants associated with complement dysregulation, many patients remain asymptomatic for most of their lives. Several conditions, including pregnancy, can precipitate episodes of TMAs, which can be mistaken for preeclampsia. Advances in complement genetics have transformed our understanding of TMAs, but interpreting complement genetics is complex and often requires expertise from geneticists and complement biology specialists. This case illustrates the need to remain vigilant about atypical obstetric complications, as adequate treatment of aHUS can prevent irreversible renal injury.