Postpartum complement-mediated thrombotic microangiopathy/atypical hemolytic uremic syndrome with active IgA nephropathy and acute tubular injury: a case report

Background Postpartum anemia, thrombocytopenia, and acute kidney injury (AKI) should raise concern for thrombotic microangiopathy (TMA). However, thrombotic thrombocytopenic purpura, complement-mediated TMA/atypical hemolytic uremic syndrome (CM-TMA/aHUS), obstetric TMA, and other secondary causes may overlap early in the course. Case presentation: A 35-year-old woman developed oliguria 5 h after cesarean delivery complicated by an estimated blood loss of approximately 1200 mL. On admission, hemoglobin was 54 g/L, platelet count 32 × 10⁹/L, serum creatinine 235.2 µmol/L, and lactate dehydrogenase 1411.3 U/L. Plasma exchange and continuous kidney replacement therapy were started while TTP was being assessed. ADAMTS13 activity was 94% with a negative inhibitor test, and complement testing showed low C3 and elevated soluble C5b-9. Eculizumab was initiated for clinically suspected postpartum CM-TMA/aHUS. Kidney biopsy showed TMA-related vascular lesions, active IgA nephropathy (Oxford M1E1S1T0-C2), and acute tubular injury. Recurrent microscopic hematuria from early pregnancy suggested that IgA nephropathy probably preceded the postpartum TMA event. The patient recovered hematologically, discontinued dialysis, and showed short-term improvement in kidney function and proteinuria after complement-directed and IgA nephropathy-directed treatment. Conclusions This case highlights the need for parallel diagnosis and treatment in postpartum TMA. Pre-existing IgA nephropathy may provide a complement-active renal background, whereas delivery, hemorrhage, infection, and coagulation disturbance may trigger or amplify CM-TMA/aHUS and tubular injury.