IgA nephropathy, the most common form of primary glomerulonephritis, progresses to terminal renal failure in about 25% of patients 10 years after the apparent clinical onset. Since its description in 1968 an intense research effort in order to clarify the pathogenetic mechanisms has involved the study of animal models of the disease. In this review we analyze the experimental work 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 relevant clinical observations. Finally, we report the new insights about the role played by cytokines and growth factors.