Glomerular and tubulointerstitial accumulation of extracellular matrix proteins is a common feature of progressive renal disease and parallels the reduction in organ function that finally necessitates dialysis or transplantation. During the last decade, studies on the pathogenesis of fibrotic renal disease have shown that both angiotensin II (Ang II) and transforming growth factor-(TGF-) play a critical role in this process. TGF-1 has been shown to directly induce both increased synthesis and reduced degradation of matrix proteins, leading to a net accumulation of pathological matrix. Angiotensin II was long thought to be merely a hemodynamic factor until it was shown by Wolf et al. and Kagami et al. that it is indeed a potent inducer of TGF-in renal tubular and mesangial cells [1, 2], thus contributing to the development of fibrosis. This review focuses on TGF-in fibrotic renal disease and its interaction with Ang II in the pathogenesis of fibrosis.