Post-miscarriage Complement-Mediated Thrombotic Microangiopathy in a 27-Year-Old Woman: A Case Highlighting Diagnostic and Therapeutic Gaps in Brazil

Thrombotic microangiopathies (TMAs) comprise a group of severe diseases characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ dysfunction. Differential diagnosis among subtypes such as complement-mediated TMA (atypical hemolytic uremic syndrome (aHUS)), thrombotic thrombocytopenic purpura (TTP), and typical hemolytic uremic syndrome (HUS) is particularly challenging in settings with limited diagnostic and therapeutic resources. We report the case of a 27-year-old patient, G2P0A1, admitted to a private Brazilian hospital at 19 weeks of gestation with a pregnancy complicated by anhydramnios and spontaneous abortion, followed by difficult-to-control bleeding and rapid clinical deterioration. After the abortion and uterine curettage, the patient developed the classic triad of thrombotic microangiopathy in addition to high fever, hypovolemic shock, severe metabolic acidosis, acute kidney injury with anuria requiring hemodialysis, significant coagulopathy, and marked elevation of transaminases. The diagnostic workup was hampered by the unavailability of key tests, such as A Disintegrin And Metalloprotease with ThromboSpondin type 1 motif, member 13 (ADAMTS13) activity and complement genetic testing. Nevertheless, the combination of (1) TMA triad, (2) reduced complement level (C3), (3) low risk of TTP according to the PLASMIC score and absence of need for plasmapheresis, (4) lack of preceding diarrhea suggestive of typical HUS, (5) negative cultures and no specific response to antimicrobial therapy, and (6) a clinical course incompatible with Hemolysis, Elevated Liver enzymes, and Low Platelets (HELLP) syndrome supported the diagnosis of complement-mediated TMA, likely triggered by obstetric complications and associated with disseminated intravascular coagulation (DIC). Twelve days after the initial event, repeat ultrasound revealed retained products of conception, and a second curettage was performed, followed by progressive clinical improvement. Despite this, the patient evolved to permanent renal failure with dialysis dependence due to lack of access to targeted therapies such as eculizumab, which could potentially have modified the prognosis. This case illustrates how, even in private hospitals, the limited availability of diagnostic tests and specific therapies compromises adequate differential diagnosis of TMAs and influences critical outcomes. It highlights the significant impact of structural barriers on the management of rare and complex diseases such as aHUS in Brazil.