The effects of dietary P restriction to half the recommended minimum level on growth, bone and renal mineralization and urinary composition were studied in female kittens. In two separate experiments, 8-week-old weanling kittens were fed on purified diets containing either 4·6 or 9·2 mmol P/MJ (2·8 or 5·6 g P/kg diet). In the second experiment there was an additional low-P diet in which the Ca concentration was reduced from 9·5 to 4·8 mmol/MJ (7·5 v. 3.8 g Ca/kg diet). P restriction slightly but systematically reduced weight gain (to a maximum of 16%) and growth of the tibia (by 1–4%); the former effect was statistically significant (P < 0·05) between the ages of 15 and 20 weeks in Expt 1 only, and the latter did not reach statistical significance at any time point (P g 0·13). No adverse effect of P restriction was found on mineralization of femur at the age of 39 weeks. Kidney Ca concentrations were significantly lowered (Expt 1, 6 v. 20/μmol/g dry weight, P < 0-001; Expt 2, 7 v. 16/μmol/g dry weight, P < 0-01) in cats fed on the low-P diets, this effect not being affected by the dietary Ca:P ratio. Urinary P concentration was significantly depressed (by 50–96%) after feeding the low-P diets (P < 0-001). P intake did not influence P, Ca and Mg retention during the period of 15 to 39 weeks of age.

Increased intakes of protein have been shown to reduce kidney calcification (nephrocalcinosis) in female rats. Two questions were addressed in the present study. First, can protein-induced inhibition of nephrocalcinosis be demonstrated when the diets used are balanced for calcium, magnesium and phosphorus in the added protein? Second, can the protein effect be explained by the frequently observed magnesiuria after giving high-protein diets? Nephrocalcinosis was induced in female rats by giving purified diets containing 151 g casein/kg and either an increased concentration of P (6 v. 2 g/kg) or a decreased concentration of Mg (0·1 v. 0·4 g/kg). To these diets 151 g ovalbumin/kg was added at the expense of glucose, and the diets were balanced for Ca, Mg and P in ovalbumin. The diets were given for 29 d. In rats fed on the diet containing 151 g protein/kg, an increased intake of P or a decreased intake of Mg caused nephrocalcinosis as measured chemically by analysis of kidney Ca as well as histologically by scoring kidney sections stained according to Von Kossa's method. The addition of ovalbumin to the diet prevented the induction of nephrocalcinosis. High P intake and low Mg intake with the low-protein diets induced enhanced loss of albumin in urine, suggesting that nephrocalcinosis caused kidney damage. Increased protein intake with a non-calcinogenic diet also caused increased albumin excretion in urine. Irrespective of the composition of the background diet, increased protein intake caused increased urinary excretion of Mg. When all dietary groups were considered, differences in nephrocalcinosis and urinary Mg output were not proportionally related.

Nephrocalcinosis: Phosphorus: Magnesium: Protein: Rat