Control of nephrocalcinosis by manipulating the calcium: phosphorus ratio in commercial rodent diets

Clapp, M. J. L.; Wade, Julie D.

doi:10.1258/002367782781110232

Cited by 40 publications

(15 citation statements)

References 6 publications

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“…Various synonyms for nephrocalcinosis include renal mineralization, mineralization of the kidney, calci cationkidney, phosphorus-induce d nephrocalcinosis, and phosphate crystals in tubules (15,16). These terms indicate that there is mineral deposition in the kidney and it appears to be associated with phosphorus and calcium.…”

Section: Nephrocalcinosismentioning

confidence: 99%

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Diet and Kidney Diseases in Rats

Rao

2002

Toxicol Pathol

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Diet-associated kidney diseases of rats includes nephropath y in both sexes and nephrocalcinosi s in females. High protein content of diets appears to be the major cause for severe nephropathy and changing the source of protein to one such as soy protein, restricting caloric intake, or modifying the diet to decrease protein consumption could decrease the severity of nephropathy. The NTP-2000 diet with lower protein content than most diets decreases the severity of nephropathy and increases the survival of Fischer 344 rats without substantial changes in growth patterns and body weights. Nephrocalcinosis , characterized by mineralization of renal tubules at the corticomedullary junction, has been reported in young and adult female rats of most strains and stocks suggesting a major contribution of female sex hormones to the developmen t of this lesion. Calcium (Ca), phosphorou s (P), magnesium (Mg), and chloride (Cl) imbalances, especially a Ca:P ratio of less than 1.0 in diet, are considered to be associated with this lesion. Most commercial diets commonly used for toxicology studies have a Ca:P molar ratio of less than 1.0. Increasing the Ca:P molar ratio to more than 1.0 and closer to 1.3 in the AIN-93 puri ed diet and NTP-2000 nonpuri ed diet prevents the developmen t of this lesion. Genetics will predispose rats to some diseases and environmental factors will in uence the severity of these diseases. Diet is one of the most important environmenta l factors. Diets balanced for nutrients without excesses could markedly improve the health of rats used in chronic studies leading to substantial increases in survival and thereby accomplish the objective of chronic toxicity and carcinogenicity studies.Keywords. Nephropathy ; nephrocalcinosis ; protein; Ca:P ratio; cardiomyopathy ; control of nephropathy ; prevention of nephrocalcinosis ; control of cardiomyopathy.Diet-associated kidney diseases of most rat strains and stocks includes nephropathy in both sexes and nephrocalcinosis mainly in females. NEPHROPATHYIn the literature, nephropathy in rats is listed under various conditions of the kidney. These include progressive renal disease, spontaneous nephrosis, chronic nephrosis, chronic progressive nephrosis, and progressive glomreulonephrosis. These pathological conditions re ect the nature and progression of the disease. Additional terms such as protein-overload nephropathy and dietary nephritis re ect the possible contribution of protein and diet to the development and progression of the disease. Some terms include nephritis and glomerulonephritis, indicating an in ammatory component to this disease; other terms including spontaneous glomerulosclerosis and glomerular hyalinosis (1, 2, 3) indicate the progression and nal outcome of this condition. Figure 1 shows the gross appearance of kidneys with moderate nephropathy, and Most strains and stocks of rats used for toxicology and carcinogenesis studies develop nephropathy. Although SpragueDawley and Wistar rats are highly susceptible and Fischer 344, Long-Eva...

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Section: Nephrocalcinosismentioning

confidence: 99%

“…These terms indicate that there is mineral deposition in the kidney and it appears to be associated with phosphorus and calcium. Nephrocalcinosis is mineralization of renal tubules at the corticomedullary junction (15,16). The histological appearance of a kidney with moderate nephrocalcinosis is shown in Figure 6.…”

Section: Nephrocalcinosismentioning

confidence: 99%

Diet and Kidney Diseases in Rats

Rao

2002

Toxicol Pathol

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“…The incorporation of high amounts of fluoride into a high phosphorus or low magnesium diet protects against nephrocalcinosis (Luoma et al, 1976;Forbes, 1971). The incidence of kidney calcification in rats fed commercial diets can vary considerably (Cousins & Geary, 1966;Clapp, 1980;Clapp et al, 1982). A study showed that in rats fed 3 out of 6 commercial rat diets there was a high incidence of nephrocalcinosis (Clapp, 1980).…”

Section: Diet and Nephrocalcinosismentioning

confidence: 99%

Nutrition and kidney calcification in rats

1989

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Nephrocalcinosis is a 'spontaneous' disorder in rats which refers to the deposition of calcium salts in the kidney, preferably in the corticomedullary region. Studies using defined, semi-purified diets have shown that low dietary concentrations of magnesium, high concentrations of calcium, high concentrations of phosphorus and low calcium: phosphorus ratios induce kidney calcification. Dietary phosphorus induced nephrocalcinosis in female rats is associated with increased kidney size and weight, tubular hyperplasia, fibrosis and increased excretion of albumin in urine. This suggests that nephrocalcinosis may impair kidney function. In rats fed different commercial diets the incidence of nephrocalcinosis can vary considerably. Differences in the degree of nephrocalcinosis in different experiments may negatively influence the comparability of experimental outcome, especially when this is affected by kidney function and structure. Experimental data are needed so that diets can be formulated that do not produce nephrocalcinosis without inducing other disorders.

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“…Concerning the latter, of prime importance is the balance between the calcium, phosphorus and magnesium content of the diet. A common feature of all diets which induce nephrocalcinosis is a calcium: phosphorus ratio of 1 or less (Du Bruyn, 1970, 1972Hitchman, Hasany, Hitchman, Harrison & Tam, 1979;Clapp, 1980;Clapp et at. 1982;Harwood, 1982).…”

Section: A K J Al-modhefer and Othersmentioning

confidence: 99%

“…Most of the commonly used rat strains are affected by the condition, and the incidence of the lesion is consistently greater in females than males (see, for example, Forbes, 1963;Geary & Cousins, 1969;Goulding & Malthus, 1969;Woodard, 1971 a, b;Du Bruyn, 1972;Kaunitz & Johnson, 1976; Clapp, 1980;Clapp, Wade & Samuels, 1982;Harwood, 1982). In nephrocalcinosis, a precipitation of calcium phosphate occurs initially in proximal tubule brush borders.…”

Section: Introductionmentioning

confidence: 99%

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

Al-Modhefer¹,

Atherton²,

Garland³

et al. 1986

The Journal of Physiology

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SUMMARY1. Single-nephron and whole-kidney function were studied in female rats with corticomedullary nephrocalcinosis, and in animals where the lesion had been prevented either by a dietary magnesium supplement or by using a diet with a calcium: phosphorus ratio in excess of 1.2. At the single-nephron level, rats with nephrocalcinosis had prolonged tubular fluid transit times. Proximal transit time was 19-42 + 1-98 (mean+ S.E. of mean) vs. 1 1-58 + 0-19 s for controls; distal transit time was 62-64 + 9-16 vs. 31-50 + 1-03 s for controls.3. Although single-nephron function is altered in nephrocalcinosis, data obtained from rats in metabolism cages indicate that whole-kidney function is largely unaffected by the lesion.

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Control of nephrocalcinosis by manipulating the calcium: phosphorus ratio in commercial rodent diets

Abstract: Changing the calcium: phosphorus ratio in 2 commercial diets from 0·73 and 0·84 to 1·25 and 1·20 reduced the incidence of nephrocalcinosis (which occurred almost entirely in female rats) virtually to nil.

Cited by 40 publications

References 6 publications

Diet and Kidney Diseases in Rats

Diet and Kidney Diseases in Rats

Nutrition and kidney calcification in rats

Kidney function in rats with corticomedullary nephrocalcinosis: effects of alterations in dietary calcium and magnesium.

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