Role of dietary factors in the progression of chronic renal disease

Klahr, Saulo; Buerkert, John; Purkerson, Mabel L.

doi:10.1038/ki.1983.197

Cited by 150 publications

(64 citation statements)

References 69 publications

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“…Replacing casein as the main protein with liver or vegetable proteins (e.g., soybean) is also protective, suggesting that the source of protein is important (Iwasaki et al, 1988a;. Dietary carbohydrate and fat, and serum lipids have also been implicated in the progression of CPN (Klahr et al, 1983;Kleinknecht et al, 1986;Iwasaki et al, 1988b), but these appear not to be the major factors involved. On the other hand, restriction of caloric intake is more powerful than any other dietary manipulation (Everitt et al, 1982;Yu et al, 1982;Bertani et al, 1989;Zawada et al, 1997;Keenan et al, 2000).…”

Section: Factors That Modify Cpnmentioning

confidence: 99%

Invited Review: A Contemporary Overview of Chronic Progressive Nephropathy in the Laboratory Rat, and Its Significance for Human Risk Assessment

Hard¹,

2004

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CPN (chronic progressive nephropathy) is a spontaneous age-related disease that occurs in high incidence in the strains of rat commonly used in preclinical toxicology studies, exhibiting a male predisposition. Although increasing in incidence and severity with age, evidence indicates that CPN should be regarded as a specific disease entity and not just a manifestation of the aging process. A number of factors, mainly dietary manipulations, have been shown to modify the expression of CPN. Amongst these, restriction of caloric intake is the most effective for inhibiting the disease process. The precise etiology of CPN and the mechanism(s) underlying its pathogenesis remain unknown, but the long-standing assumption that glomerular dysfunction is the primary basis is challenged in the light of contemporary developments in understanding filtration and postglomerular cellular processing of albumin. CPN is not only a degenerative disease, but also has regenerative aspects with a high cell proliferative rate in affected tubules. Accordingly, evidence is emerging that advanced, particularly end-stage CPN, is a risk factor for a marginal increase in the background incidence of renal tubule tumors. Many chemicals are known to exacerbate the severity of CPN to an advanced stage, and this interaction between chemical and CPN can result in a small increase in the incidence of renal adenomas in 2-year carcinogenicity bioassays. Review of the pathological entities associated with chronic renal failure in man emphasizes that this rodent condition has no strict human counterpart. Because CPN is a rodent-specific entity, the finding of a small, statistically significant increase in renal tubule tumors, linked to exacerbation of CPN by a test chemical in a preclinical study for carcinogenicity, can be regarded as having no relevance for extrapolation in human risk assessment.

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Section: Factors That Modify Cpnmentioning

confidence: 99%

Invited Review: A Contemporary Overview of Chronic Progressive Nephropathy in the Laboratory Rat, and Its Significance for Human Risk Assessment

Hard¹,

2004

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“…There have been many reports that protein restriction delays the progression of chronic renal failure (CRF) in both experimental uremic rats (1,2) and undialyzed uremic patients (3,4). To date, various possible mediators of the effect of dietary protein on the progression of renal insufficiency have been indicated, including angiotensin II (5,6), transforming growth factor-␤ (7), eicosanoids (8), and glucocorticoids (9,10).…”

mentioning

confidence: 99%

Role of Organic Anion Transporters in the Tubular Transport of Indoxyl Sulfate and the Induction of its Nephrotoxicity

Enomoto

Takeda

Tojo³

et al. 2002

Journal of the American Society of Nephrology

276

204

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Abstract. In uremic patients, various uremic toxins are accumulated and exert various biologic effects on uremia. Indoxyl sulfate (IS) is one of uremic toxins that is derived from dietary protein, and serum levels of IS are markedly increased in both uremic rats and patients. It has been previously reported that the accumulation of IS promotes the progression of chronic renal failure (CRF). This study demonstrates the role of rat organic anion transporters (rOATs) in the transport of IS and the induction of its nephrotoxicity. The administration of IS to 5/6-nephrectomized rats caused a faster progression of CRF, and immunohistochemistry revealed that IS was detected in the proximal and distal tubules where rOAT1 (proximal tubules) and/or rOAT3 (proximal and distal tubules) were also shown to be localized. In in vitro study, the proximal tubular cells derived from mouse that stably express rOAT1 (S2 rOAT1) and rOAT3 (S2 rOAT3) were established. IS inhibited organic anion uptake by S2 rOAT1 and S2 rOAT3, and the Ki values were 34.2 and 74.4 M, respectively. Compared with mock, S2 rOAT1 and S2 rOAT3 exhibited higher levels of IS uptake, which was inhibited by probenecid and cilastatin, organic anion transport inhibitors. The addition of IS induced a decrease in the viability of S2 rOAT1 and S2 rOAT3 as compared with the mock, which was rescued by probenecid. These results suggest that rOAT1 and rOAT3 play an important role in the transcellular transport of IS and the induction of its nephrotoxicity.

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“…A literature review by Klahr et al (1983) of experimental studies in animais and humans clearly depicts that excessive dietary protein intake accelerates progression of renal diseases. High protein intake is known to increase renal blood tlow and GFR producing hyperperfusion and hyperfiltration while the mechanisms by which low protein intake attenuates kidney disease are not clear yet.…”

Section: Dietary Proteinsmentioning

confidence: 99%