The question was addressed whether dietary phosphorus-induced nephrocalcinosis in rats is associated with impaired kidney function. Weanling female rats were fed purified diets containing either 0.4 or 0.6% (wt/wt) phosphorus for 28 d. The diet containing 0.6% phosphorus produced marked kidney calcification, as determined both by chemical analysis of kidney calcium and histological examination in kidney sections. Histological examination did not show calcification in stomach, lung, heart or thoracic aorta, which are predisposition sites of metastatic calcification in secondary renal hyperparathyroidism. In rats fed the 0.6% phosphorus diet, phosphorus retention and urinary excretion were greater compared with rats fed the 0.4% phosphorus diet. The following indicators of kidney function were examined: water intake, urinary volume, urine and plasma osmolality, urine and plasma creatinine, urine and plasma urea, urea and creatinine clearance and urinary albumin excretion. Of these indicators, only urinary albumin excretion was significantly increased in rats fed the nephrocalcinogenic diet. In a further experiment, the increase of urinary albumin was reproduced. After pooling the results of the two experiments, in individual rats fed the 0.6% phosphorus diet, the concentration of kidney calcium was found to be positively related with kidney weight expressed relative to body weight (r = 0.82, n = 22) and with albumin excretion in urine (r = 0.79, n = 28). The increased weight of calcinotic kidneys was mainly due to both calcium deposition and tubular hyperplasia. It is concluded that dietary phosphorus-induced nephrocalcinosis is associated with impaired kidney function in rats.

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Yellow fat disease was induced in young rats given a vitamin E-deficient diet supplemented with 15% fish oil. The changes in adipose tissue of this oil-induced disorder were different from those of natural yellow fat disease in horse, pig and mink. In the natural disease all fat depots had the early stage of yellow fat disease with interstitial lipofuscin-laden macrophages exclusively. In the rat, however, this change was seen only in the subcutaneous fat depot. Moreover, affected adipose tissue of animals with natural disease had extensive fibrosis, but in the rat fibrosis was always absent. Rats with fish oil-induced yellow fat disease had degenerative changes in various fat depots that occurred at various times but in the horse, pig and mink fat depots were affected simultaneously. Lipofuscin accumulated in the reticuloendothelial system in rats. Accumulation in spleen and liver was dependent on vitamin E deficiency, but only the accumulation in the Kupffer cells was correlated with yellow fat disease. Lipofuscin accumulation in the mesenteric lymph node did not depend on vitamin E deficiency.

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In a long-term experiment with three successive generations of rats, the influence of dietary phosphorus restriction (2 instead of 4 g phosphorus/kg diet) on nephrocalcinosis, reproduction and bone mineralization was studied. Nephrocalcinosis in female rats, as based on kidney calcium concentration and histological examination, was prevented by phosphorus restriction. The low phosphorus diet caused reduced femur concentrations of magnesium, calcium and phosphorus in rats of the first and second generation aged 4 to 12 wk. The low phosphorus diet resulted in lower plasma phosphorus concentrations. In the kidneys of female rats, immediately after lactation, a higher degree of tubular hyperplasia was seen after the low phosphorus diet was fed. Reproductive performance was not affected by phosphorus restriction. We conclude that 0.2% phosphorus in the diet prevents nephrocalcinosis in female rats while it sustains reproduction but delays bone mineralization.