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The results of experimental studies and clinical trials have identified blockade of the renin angiotensin system (RAS) as a cardinal way of arresting the progression of renal disease to end-stage failure (1). Slowing the rate of progression has been the key goal until recently; however, current approaches have already taken additional steps forward by looking at ways to halt progression and even promote increases of GFR over baseline values and improvement of associated structural in- jury, that is to achieve regression of renal disease. The rationale for such approaches rests on two basic considerations. First, many forms of chronic nephropathy evolve to end-stage through a series of events that are relatively independent of the initial insults that cause parenchymal damage when the injury affects a critical number of nephrons. Blocking the common pathway(s) of injury by angiotensin blockade could then spare renal structures from damage via angiotensin II, maladaptive mechanisms, and protein trafficking. Still more open was the possibility that drug therapies may eradicate certain structural components of injury that are usually believed to be inevitably irreversible, thus fully protecting renal function and minimiz- ing the risks of evolutive disease. Experimental lines of evidence have suggested that such possibility is credible and worth investigating further. The background again can be derived from seminal studies using low-protein diet or angiotensin I- converting enzyme inhibitors (ACE-I), the first ones to show that the glomeruli can be protected against the development of sclerosis in rats with progressive nephropathy due to extensive reduction of renal mass or streptozotocin diabetes (2). Compared with a non- ACE-I regimen that achieved equivalent systemic BP control, ACE-I better reduced renal injury partially via amelioration of glomerular hypertension. Recent years have yielded convinc- ing demonstration that both glomerulosclerosis and chronic tubulointerstitial injury, once developed, can be stabilized and even revert. In Munich Wistar Fromter (MWF) rats with spon- taneous disease, ACE-I given late during the animal's life, when animals were already heavily proteinuric, decreased pro- teinuria and stopped the disease from progressing, as docu- mented by a lower incidence of glomeruli affected by sclerotic lesions and less interstitial injury than in untreated controls (3). In few studies of other models, the disease was usually not

Can We Really Lessen Kidney Damage to the Point that the Loss of Renal Function of Progressive Nephropathy May Revert?