Pharmacological management of renal fibrotic disease

Chronic kidney diseases frequently advance to end-stage renal failure, and the number of patients affected is steadily increasing worldwide. At the molecular level, progression of renal insufficiency correlates closely with ongoing pathological matrix protein expansion (i.e., renal fibrosis), in a manner independent of the underlying disorder. Overactivity, of the reninangiotensin system and of the TGF-beta system have been identified as key mediators of kidney matrix accumulation, and are principal targets in the management of chronic renal disease. This review provides a recent overview of the therapeutic options that are clinically established, and of novel molecular strategies that will approach clinical practice in the near future.