Role of dietary factors in the progression of chronic renal disease

In diseases of the kidney characterized by irreversible injury, it appears that once a critical level of renal functional deterioration is reached, progression to endstage disease invariably occurs even if the initiating event or condition is resolved or eradicated. Immunopathogenetic mechanisms probably account for most forms of primary glomerular disease in humans. Although immunologic events and the mediators of glomerular damage that they induce might be responsible for initiating most glomerular diseases, certain clinical and experimental observations suggest that the rate of progression of these diseases is influenced by several nonimmunologic factors. In certain diseases, such as proliferative glomerulonephritis, the relentless decrease in renal function is due very likely to the initial underlying process; in other entities characterized mainly by interstitial scarring and glomerular sclerosis, the cause of progressive loss of renal function is less apparent. Recent experimental evidence suggests that dietary manipulations, such as reductions in protein and/or phosphate intake, can halt or attenuate the progression of chronic renal insufficiency in experimental animal models. Therefore, the exciting possibility exists that the natural history of some renal diseases may be altered by changes in the diet. We review current information regarding the role of manipulations of dietary protein, phosphorus, or lipid content on the progression of chronic renal disease. Most of the experimental observations to be reviewed have been made in animal models of renal disease. The literature on the role of dietary manipulations on the progression of renal disease in patients is somewhat limited and will not be emphasized here.