Much study has been dedicated to the understanding of the mechanisms leading to the progression of renal injury and to the development of strategies to limit this progression or possibly induce tissue regeneration. Among several identified mechanisms, the role of angiotensin II is widely recognized. Moreover, the progression of glomerular damage is characterized by capillary loss, reduction of the proliferative response, and production of antiangiogenic factors. Several lines of evidence support the potential effect of therapeutic startegies aimed at interfering with angiotensin II or stimulating angiogenesis in order to reduce the progression of renal injury. Recent work has underlined the potential of strategies involving the use of stem cells. Different populations of stem cells have been identified in the adult kidney. During renal injury, stem cells derived from the bone marrow that migrate through the circulation to the kidney may contribute to tissue repair. The regenerative potential of stem cells could be exploited by administration of ex vivo expanded stem cell populations or by the development of techniques to expand and differentiate local stem cells.