Renal toxicity of phosphate in rats.

@article{Haut1980RenalTO,
  title={Renal toxicity of phosphate in rats.},
  author={Lindsey Haut and Allen C. Alfrey and S P Guggenheim and B Buddington and Nick Schrier},
  journal={Kidney international},
  year={1980},
  volume={17 6},
  pages={
          722-31
        }
}
To evaluate the mechanism by which phosphate induces renal injury, we placed uninephrectomized, partially nephrectomized, and intact rats on dietary phosphorus intakes varying between 0.5 and 2% for 18 weeks. None of the animals on a normal phosphorus intake (0.5%) had any abnormalities. Four out of six intact animals on a 1% phosphorus diet had kidney calcium concentrations within the normal range, and only one showed any histologic changes. In contrast, all but one partial and… 

Prevention of phosphate-induced progression of uremia in rats by 3-phosphocitric acid.

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Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. I. Renal function and biochemical changes.

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At 30 days of renal failure, NH( 4)Cl ingestion increased creatinine and urea clearances, irrespective of dietary phosphorus; high urine calcium excretion, induced by dietary phosphorus restriction and NH(4)Cl ingested, did not adversely affect renal function; high dietary phosphorus did not decrease renal function.

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Following 5/6 nephrectomy, 18 rats were fed a normal diet and when serum phosphorus (SPi) and serum calcium (SCa2+) were normal, the rats were separated into two groups, matched and paired by body weight and SCr, and housed separately in metabolic cages.

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It is concluded that high dietary protein can accelerate the development of glomerular injury independent of effects onglomerular hemodynamics.

Dietary protein prior to renal ischemia dramatically affects postischemic kidney function.

TLDR
It is found that approximately a week on this diet is necessary to provide maximum protection from postischemic acute renal failure, and suggests that preoperative dietary protein intake should be an important consideration in those situations which are predisposed to postoperative acute kidney failure.

Chronic metabolic acidosis in azotemic rats on a high-phosphate diet halts the progression of renal disease.

TLDR
The presence of chronic metabolic acidosis in 5/6 nephrectomized rats on a high-phosphate diet protected against the progression of RF, enhanced the renal clearance of phosphate, resulted in a lesser degree of hyperparathyroidism, and did not reduce the osteoblast surface.

Sevelamer hydrochloride, a phosphate binder, protects against deterioration of renal function in rats with progressive chronic renal insufficiency.

  • N. NaganoS. Miyata M. Wada
  • Medicine, Biology
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • 2003
TLDR
The results suggest that sevelamer protects against renal function deterioration by maintaining kidney calcium at a low level as a result of reducing serum phosphorus and PTH.

The role of dietary protein in progressive renal disease.

  • B. Brouhard
  • Medicine, Biology
    American journal of diseases of children
  • 1986
TLDR
Patients with progressive renal disease of various causes, when placed on low-protein diets, exhibit a slowing of the decline in renal function, and whether reduced protein intake is needed during times of physiologic increases in GFR (pregnancy, unilateral nephrectomy) is not clear.

Dietary Phosphate Restriction Attenuates Polycystic Kidney Disease in Mice.

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Dietary phosphate restriction slows cystogenesis and inhibits the activation of key pathways in the generation of kidney fibrosis in PKD mice.
...

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