As an autoimmune disease, IgA nephropathy is pathologically characterized by the deposition of immunoglobulin A (IgA) in the glomerular mesangial area. Recent research has confirmed that the activation of the lectin pathway in the complement system may be related to the development and prognosis of IgA nephropathy (IgAN). These deposited immune complexes trigger the complement cascade, generating various inflammatory mediators that directly attack glomerular mesangial cells and promote mesangial matrix proliferation and crescent formation, ultimately leading to end stage renal disease. Therefore, an in-depth understanding of complement activation pathways not only provides potential non-invasive biomarkers (such as urinary complement components) for assessing disease activity and prognosis, more importantly, establishes a theoretical foundation for developing novel anti-complement targeted therapies. This holds promise for opening new directions in the personalized precision treatment of IgA nephropathy. This article reviews the research progress on the lectin pathway and its associated components in IgA nephropathy.
Yu et al. (Fri,) studied this question.