Abstract
The presence of albuminuria has long been recognized as an adverse prognostic feature in patients with renal disease. Those patients with appreciable albuminuria are much more likely to develop tubulointerstitial scarring and fibrosis and progress to end-stage renal failure. For many years it was thought that excess albuminuria was simply a marker of a more severe renal disease which was more likely to progress as a result of this severity rather than as a result of the albuminuria itself. This conviction was strengthened by the general assumption that albumin was a benign or inert molecule serving primarily to exert oncotic pressure and act as a carrier within the circulation.
More recently this view has been challenged with the accumulation of evidence suggesting that albumin is able to influence the function of cells with which it makes contact in the manner of a signaling molecule.