Renal toxicity of phosphate in rats.

@article{Haut1980RenalTO,
  title={Renal toxicity of phosphate in rats.},
  author={L L 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… Expand
Prevention of phosphate-induced progression of uremia in rats by 3-phosphocitric acid.
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3-phosphocitric acid, a compound which has been shown to prevent calcium phosphate crystal growth as well as to prevent in vivo nephrocalcinosis, was very effective in preventing this phosphate-induced deterioration of renal function and in preventing any significant increase in renal calcium content in animals fed a high phosphate diet. Expand
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. Expand
Effect of ammonium chloride and dietary phosphorus in the azotaemic rat. Part II--Kidney hypertrophy and calcium deposition.
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NH(4)Cl and dietary phosphorus each independently affect kidney growth and calcium deposition in the growing rat with renal failure and suggests that kidney hypertrophy does not completely compensate for the harmful effects of a HPD. Expand
tciry Mineral Restriction in Do 9 s with Marked Reduction of Functional Renal Mass 1 ’ 2
Although studies in partially nephrectomized rats have identified a progressive nephropathy that is altered by dietary restriction of phosphorus intake, the response of dogs to similar perturbationsExpand
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The hypothesis that ingestion of large amounts of dietary protein leads to sustained renal hyperperfusion and progressive glomerulosclerosis in rats is not supported and results do not support the hypothesis that high protein feeding had a significant adverse effect on either renal function of morphology in dogs with 75% nephrectomy. Expand
Phosphate depletion arrests progression of chronic renal failure independent of protein intake.
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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. Expand
High protein intake accelerates glomerulosclerosis independent of effects on glomerular hemodynamics.
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It is concluded that high dietary protein can accelerate the development of glomerular injury independent of effects onglomerular hemodynamics. Expand
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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. Expand
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. Expand
Sevelamer hydrochloride, a phosphate binder, protects against deterioration of renal function in rats with progressive chronic renal insufficiency.
  • N. Nagano, S. Miyata, +4 authors M. Wada
  • Medicine
  • 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. Expand
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Dietary restriction of phosphorus retards functional deterioration and reduces histologic damage in experimental immunologic renal disease and survival was markedly improved in group B animals. Expand
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The results suggest that the calcification produced by the altered phosphorus metabolism present in the uremic state incites an inflammatory and fibrotic reaction leading to destruction of the remnant kidney. Expand
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Dietary phosphorus-dependent alterations in Pi reabsorption may play a significant role in establishing the rate of Pi excretion per nephron under certain circumstances and should be considered in the interpretation of studies investigating renal Pi handling. Expand
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TLDR
Results indicate that factors other than parathyroid hormone are implicated in the tubular response to variations in the dietary intake of inorganic phosphate, and tubular reabsorption of phosphate (TRPi) could be assessed over a wide range of plasma phosphate concentrations. Expand
RENAL DAMAGE FOLLOWING THE INGESTION OF A DIET CONTAINING AN EXCESS OF INORGANIC PHOSPHATE
The addition of an excess of inorganic phosphate in the form of orthophosphoric acid, acid, basic or neutral sodium or potassium phosphate to the diet of albino rats results in the development of anExpand
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TLDR
Clearance studies indicate that, in anaesthetized rats, the net tubular reabsorption decreases markedly in response to Pi infusion, and microperfusions of proximal tubules show a fall in the specific radioactivity of the perfused radioactive Pi solution, indicating entry of Pi into the lumen. Expand
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TLDR
This investigation was undertaken to study the effect of feeding diets containing varying concentrations of dried yeast on renal hypertrophy, renal function and blood pressure in intact and in partially nephrectomized rats. Expand
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TLDR
Stable serum phosphate levels and increased fractional excretion of phosphate in response to a decrease in GFR were demonstrated in acutely TPTX dogs who were not receiving vitamin D, indicating that phosphate homeostasis can be maintained in renal failure in the total absence of parathyroid hormone secretion. Expand
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TLDR
It is reported that variations in dietary Pi cause a much greater change in the tubular capacity to transport Pi than removal of the thryoparathyroid glands. Expand
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TLDR
Phosphate supplementation appears to result in secondary hyperparathyroidism and to cause soft-tissue calcification. Expand
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