Renal toxicity of phosphate in rats.

  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},
  volume={17 6},
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.

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.

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

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.

Effects of dietary phosphorus concentration and phosphate salt form on renal tubule function in unilateral nephrectomized rats.

This study highlights the importance of controlling dietary P intake in terms of both concentration and source to prevent the progression of CKD and shows significantly lower creatinine clearance and higher albumin compared with those of sham rats, confirming UNx-induced kidney injury.

Phosphate depletion arrests progression of chronic renal failure independent of protein intake.

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.

High protein intake accelerates glomerulosclerosis independent of effects on glomerular hemodynamics.

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.

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.

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
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
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.

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



Preservation of renal function in experimental glomerulonephritis.

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.

Preservation of function in experimental renal disease by dietary restriction of phosphate.

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.

Influence of dietary phosphorus on renal phosphate reabsorption in the parathyroidectomized rat.

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.

Inorganic phosphate homeostasis. Renal adaptation to the dietary intake in intact and thyroparathyroidectomized rats.

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.


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 an

Secretion of inorganic phosphate in the rat nephron.

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.


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.

Renal tubular adaptation to dietary phosphorus

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.

Effect of phosphate supplements on soft-tissue calcification and bone turnover.

Phosphate supplementation appears to result in secondary hyperparathyroidism and to cause soft-tissue calcification.