IgA nephropathy is the most common form of primary glomerulonephritis worldwide. About one quarter of patients progress to terminal renal failure 10 years after the apparent clinical onset. Therefore, the disease represents a social problem in terms of number of patients requiring maintenance hemodialysis. Despite the intense research effort devolved to clarify the pathogenesis of IgA nephropathy, the exact relationship linking the several factors involved is still unknown. In this review we analyze the experimental works reported since 1979, when the first animal model of IgA nephropathy was published by Rifai et al. We also discuss the interplay between experimental data and clinical observations to maximize the information gathered from the different animal models. Finally, we report the new insights into the role played by cytokines, growth factors and autacoids.