IgA nephropathy pathogenesis is incompletely understood, and this limits the development of disease-specific biomarkers and effective therapies. Evidence of complement activity in IgA nephropathy is well established. However, a growing body of research indicates complement activity is an important contributor to IgA nephropathy pathology. In particular, multiple associations have been identified between complement alternative, lectin and terminal pathway proteins and IgA nephropathy severity. Recently, we have also gained insight into possible mechanisms that could link glomerular IgA deposition, complement activity, glomerular inflammation and disease severity. Ongoing clinical trials of therapeutic complement inhibitors will provide insight into the importance of complement activity to IgA nephropathy pathogenesis. Further research into mechanisms of complement activity is essential to improving our understanding and management of patients with IgA nephropathy.

IgA 肾病的发病机制尚不完全清楚，这限制了疾病特异性生物标志物和有效疗法的发展。IgA 肾病中补体活性的证据已经确立。然而，越来越多的研究表明补体活性是 IgA 肾病病理学的重要贡献者。特别是，已确定补体替代、凝集素和末端途径蛋白与 IgA 肾病严重程度之间存在多种关联。最近，我们还深入了解了可能将肾小球 IgA 沉积、补体活性、肾小球炎症和疾病严重程度联系起来的机制。正在进行的治疗性补体抑制剂临床试验将深入了解补体活性对 IgA 肾病发病机制的重要性。