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In recent years, evidence has accumulated suggesting that early dietary intervention in the form of protein restriction can dramatically alter the natural history of chronic renal insufficiency. This article reviews the literature in this area and summarizes the questions that remain for future investigators to answer. Interest in the role of protein intake in renal disease dates back to the early 1900s, when several investigators found that the progression of renal failure was accelerated in rats and rabbits fed high-protein diets. Subsequent work in animal models has demonstrated that nephron loss, resulting from a variety of disease states, is associated with elevated intraglomerular pressures and flows. Several investigators now have postulated that these abnormal hemodynamics, resulting from intrarenal vasodilation and hyperperfusion, damage the glomerulus and may produce further nephron loss independent of the initial renal insult. Dietary protein restriction appears to reduce these pressures and flows towards normal in animals, although the operative mechanism has yet to be identified. Limited studies of dietary protein restriction in human renal disease have suggested a beneficial effect, but carefully controlled prospective studies will be necessary to establish clear therapeutic efficacy.

作者:K R, Zeller

来源:The American journal of the medical sciences 1987 年 294卷 5期

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作者:
K R, Zeller
来源:
The American journal of the medical sciences 1987 年 294卷 5期
In recent years, evidence has accumulated suggesting that early dietary intervention in the form of protein restriction can dramatically alter the natural history of chronic renal insufficiency. This article reviews the literature in this area and summarizes the questions that remain for future investigators to answer. Interest in the role of protein intake in renal disease dates back to the early 1900s, when several investigators found that the progression of renal failure was accelerated in rats and rabbits fed high-protein diets. Subsequent work in animal models has demonstrated that nephron loss, resulting from a variety of disease states, is associated with elevated intraglomerular pressures and flows. Several investigators now have postulated that these abnormal hemodynamics, resulting from intrarenal vasodilation and hyperperfusion, damage the glomerulus and may produce further nephron loss independent of the initial renal insult. Dietary protein restriction appears to reduce these pressures and flows towards normal in animals, although the operative mechanism has yet to be identified. Limited studies of dietary protein restriction in human renal disease have suggested a beneficial effect, but carefully controlled prospective studies will be necessary to establish clear therapeutic efficacy.