IgA Nephropathy: Current Understanding and Perspectives on Pathogenesis and Targeted Treatment

Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, with varied clinical and histopathological features between individuals, particularly across races. As an autoimmune disease, IgAN arises from consequences of increased circulating levels of galactose-deficient IgA1 and mesangial deposition of IgA-containing immune complexes, which are recognized as key events in the widely accepted multi-hit pathogenesis of IgAN. The emerging evidence further provides insights into the role of genes, environment, mucosal immunity and complement system. These developments are paralleled by the increasing availability of diagnostic tools, potential biomarkers and therapeutic agents. In this review, we summarize current evidence and outline novel findings in the prognosis, clinical trials and translational research from the updated perspectives of IgAN pathogenesis.

Automated summary

Immunoglobulin A nephropathy (IgAN) is a common kidney disease with different features among individuals, particularly across races. It is caused by increased levels of galactose-deficient IgA1 and deposition of IgA-containing immune complexes in the kidneys. Recent evidence suggests the involvement of genes, environment, mucosal immunity, and the complement system. This review summarizes current knowledge and new findings in the prognosis, clinical trials, and translational research of IgAN.