Effective use of a TGF- beta antagonist to treat or to prevent loss of renal function is described herein. Contrary to current theory that suggests TGF- beta antagonists may be useful in the treatment of fibroproliferative disorders of the glomeruli, no significant differences in cortical hypertrophy, and specifically glomerular injury, was observed in a genetic animal model of hypertension and renal dysfunction treated with an anti-TGF- beta antagonist compared to control animals. In contrast, the present invention demonstrates the importance of proper medullary function, and specifically the role of medullary hypoxic injury in the onset and progression of diseases and disorders of the kidney. Disclosed herein is the first demonstration that a TGF- beta antagonist is useful to effectively prevent loss of renal vascular circulation and reduce tubular injury of the renal medulla, as well as prevent systemic hypertension. Anti-TGF- beta treated animals exhibited significantly lower mean arterial pressure, significantly lower fibrosis of the vasa recta, significantly lower medullary tubular injury, significantly lower medullary tubular necrosis, and significantly higher medullary blood flow compared to control animals.
