Abstract
Since the 1980s the concept that chronic renal failure (CRF) progresses linearly and that the factors affecting progression may be separate from those initiating renal disease has dominated nephrology. In particular, the idea that hyperfiltration, rather than being a compensatory increase in the single nephron glomerular filtration rate (SNGFR) of surviving nephrons, was also the cause of their eventual demise, has thrown suspicion onto dietary protein as a factor sustaining progression. Much of the evidence rests on rats. This review concentrates on the evidence from humans and dogs and concludes that phosphate and glomerular hypertension, rather than protein are likely to accelerate progression. More important, self-sustaining progression is probably a terminal feature of CRF rather than the prevalent influence on its course. CRF is probably the result of a variety of cumulative renal insults and greater insight is therefore likely to come from the study of spontaneous renal diseases in animals, rather than contrived models.