#4808 DIFFERENTIATING POSTPARTUM HELLP SYNDROME FROM ATYPICAL HEMOLYTIC UREMIC SYNDROME

Abstract Background and Aims HELLP (hemolysis, elevated liver enzymes, low platelets) is a severe variant of preeclampsia whose pathogenesis remains unknown but likely involves abnormal placentation, endothelial dysfunction release vasoactive substances. Complement dysregulation implicated in the atypical hemolytic uremic syndrome (aHUS) there growing evidence to support its role syndrome. Here we present case postpartum thrombotic microangiopathy (TMA) setting Method We report. Ethics approval was obtained by Queen's University Health Sciences Affiliated Teaching Hospitals Research Board. Results A 22 year old G1P1 Caucasian woman presents at 37 weeks gestation with abdominal pain hypertension. Labs demonstrated TMA including hemoglobin 95, platelets 30, LDH 2597, schistocytes. She had transaminitis AST 1845 ALT 830, proteinuric acute kidney injury. diagnosed treated anti-hypertensives emergency Caesarean section. Unfortunately, infant did not survive, no placental abruption. Platelets recovered day 5 postpartum, 7. However, renal function worsened 6 she required hemodialysis. biopsy revealed chronic TMA. have cortical necrosis. Further workup normal C3, C4 ADAMTS13 levels. Dialysis stopped after two weeks. By months, her proteinuria returned normal. testing negative complement factor H autoantibody, soluble C5b-9 (sC5b-9) level (0.42 mg/L, <0.3). Ex-vivo serum deposition on human microvascular cells assessed both resting (182%, <150%) ADP-activated (273%, <150%). This test repeated months when normalized, results were persistently (215%, (282%, aHUS genetic negative. Conclusion from Burwick et al suggest that this patient very high likelihood clinical association (elevated >1832 U/L creatinine >1.9 mg/dL) [1]. Identifiable mutations only occur 50% patients. routinely for HELLP; however, severity prompted further investigation (C5b-9 testing). The persistence increased mimics findings patients who confirmed [2]. Our patient's unique may be risk recurrent TMA/aHUS lifetime, particularly if another pregnancy being considered. Future research should explore which associated benefit anti-complement therapy.