Subject(s)
Cattle Diseases/diagnosis , Deficiency Diseases/veterinary , Minerals/analysis , Vitamin E/analysis , Animals , Cattle , Cattle Diseases/blood , Cattle Diseases/metabolism , Copper/analysis , Copper/deficiency , Deficiency Diseases/diagnosis , Liver/chemistry , Manganese/analysis , Manganese/deficiency , Nutrition Assessment , Nutritional Status , Ontario , Reference Values , Selenium/analysis , Selenium/deficiency , Vitamin E Deficiency/diagnosis , Vitamin E Deficiency/veterinaryABSTRACT
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 uninephrectomized animals on a 1% phosphorus diet had increased kidney calcium content concentration, and five of the six studied had histologic changes. The degree of calcification and histologic changes in the uninephrectomized animals on a 1% phosphorus diet was similar to that found in the intact animals on a 2% phosphorus diet. Animals on a 3% phosphorus diet plus disodium ethane-1-hydroxy-1-1-diphosphonate (EHDP) had significantly less calcification and histologic changes than did animals on a similar diet without EHDP. Conclusion. As renal functional mass is reduced, the nephrotoxicity of phosporus is greatly enhanced. Phosphorus-induced renal injury is mediated through calcium phosphate deposition in the kidney. This results from intrarenal caused, because the kidney calcification can be related to phosphate excreted per functional unit rather than plasma phosphate concentrations.
Subject(s)
Kidney/drug effects , Phosphates/adverse effects , Animals , Calcinosis/chemically induced , Calcium Phosphates/metabolism , Diet/adverse effects , Diphosphonates/adverse effects , Diphosphonates/metabolism , Kidney/metabolism , Kidney/pathology , Male , Phosphates/metabolism , RatsABSTRACT
To evaluate the protective effect of dietary phosphorus restriction in an immunologic model of experimental renal disease, we randomized 24 Sprague-Dawley rats with established nephrotoxic serum nephritis into two groups. Group A animals (N = 13) were fed a diet with a normal phosphorus content (0.5% phosphorus), and group B animals (N = 11) received an identical diet low in phosphorus (0.04% phosphorus). Over the ensuing 133 days, group A rats developed progressive renal failure and had a mean serum creatinine concentration of 3.0 +/- 0.5 mg/dl at the time of death or completion of the study. In contrast, group B animals maintained near normal renal function and had a final mean serum creatinine concentration of 0.93 + 0.2 mg/dl (P < 0.001). Survival was markedly improved in group B animals (P < 0.001). Histologic damage was diminished greatly in group B animals by both light and electron microscopy; immunofluorescence was positive in all animals. Group A animals had increased kidney calcium concentration (30 +/- 6 mmoles/kg) when compared to group B animals (18 +/- 1 mmoles/kg) and animals with normal kidneys (13 +/- 1 nmoles/kg, P< 0.001). Conclusion. Dietary restriction of phosphorus retards functional deterioration and reduces histologic damage in experimental immunologic renal disease. The mechanism for this protective effect has not been elucidated.
