IgA nephropathy (IgAN) encompasses different pathological entities, all of which are characterized by the mesangial deposition of IgA. Aberrantly glycosylated IgA molecules appear to play a major role in the pathogenesis of IgAN. Both genetic and environmental factors contribute to the formation of IgG antibodies that binds to aberrantly glycosylated IgA molecules and the glomerular deposition of circulating polymeric IgA complexes. Mesangial cells serve as primary glomerular cell type injured in IgAN with a variety of pathological changes leading to progressive renal dysfunction. Recent evidence suggests that indirect podocyte injury also contributes to glomerular damage observed in IgAN. These mechanisms were demonstrated in cultured podocytes exposed to mesangial cell-conditioned medium of human IgAN. Large-scale biopsy series of human kidneys also suggest that podocyte injury plays a role in IgAN. In this review, we discuss the recent advances that have helped elucidate the mechanisms of podocyte injury in IgAN and how these mechanisms correlate with clinically important outcomes in human studies.