Coexistence of Atypical Hemolytic Uremic Syndrome and Immunoglobulin A (IgA) Nephropathy Without Readily Detectable Glomerular C3 Deposition: A Case Report

Atypical hemolytic uremic syndrome (aHUS) is a rare, life-threatening thrombotic microangiopathy in which uncontrolled activation of the complement alternative pathway (AP) plays a central role in disease pathogenesis.Immunoglobulin A (IgA) nephropathy (IgAN), another disease associated with complement activation, is the most common primary glomerular disease worldwide.The coexistence of aHUS and IgAN appears to be rare.Previous studies have hypothesized that pathological IgA in IgAN may induce persistent AP activation, thereby contributing to aHUS development.We herein report a 27-year-old woman presenting with malignant hypertension and severe renal impairment.Her clinical and histological findings supported a diagnosis of aHUS with coexisting IgAN.However, immunofluorescence revealed no detectable glomerular C3 deposition despite the severe clinical presentation.Following combined treatment with the humanized anti-C5 monoclonal antibody eculizumab, corticosteroids, and blood pressure control, the patient showed substantial hematologic and renal improvement over approximately eight months of followup and remained dialysis-independent.This case highlights an unusual pathological finding in patients with coexisting aHUS and IgAN and underscores the need for further studies to clarify the mechanisms underlying this coexistence.