Low Phosphorus Intake Research Articles

Growth and body composition of preterm infants: influence of nutrient fortification of mother's milk in hospital and breastfeeding post-hospital discharge.

We examined the influence of multi-nutrient fortification of mother's milk (MM + MNF) compared to supplementation with calcium and phosphorus (MM + CaGP) alone in hospital (in a randomized trial), and of breastfeeding (post-MM) compared to formula feeding (post-FF ) after hospital discharge with a descriptive analysis of growth and body composition to 1 y corrected age in preterm infants. Anthropometry, nutrient intakes and whole body bone mineral content, lean and fat mass were determined at four time points in the first year after term corrected age. Body composition was determined with dual energy X-ray absorptiometry. MM + MNF compared to MM + CaGP for preterm infants in the early neonatal period did not appear to influence growth or body composition in the first year. Growth in post-MM and post-FF groups was within the normal range of growth references derived from term infants fed mother's milk. Post-MM infants had lower whole body bone mineral content (132.3 +/- 10.4 g) at 6 months corrected age when compared to post-FF infants (159.4 +/- 14.1 g) and greater percent fat mass to 12 months corrected age. These differences may result from the lower calcium, phosphorus and protein intakes in post-MM compared to post-FF infants. Our findings demonstrate that dietary practices after hospital discharge likely have a greater impact on body composition in prematurely born infants than dietary practices in hospital. Whether the observed differences in body composition between breastfed and formula-fed preterm infants have any long-term consequences requires further investigation.

Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus

We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1-2g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n = 17) and patients with low BFR (group 2; n = 23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P < 0.001), osteoblast surface (P < 0.02-P < 0.01) and plasma parathyroid hormone (iPTH) (P < 0.01) increased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P < 0.02) (2b). In group 2a plasma phosphorus was below that in group 2b patients, before (P < 0.03) and after (P < 0.01) DFO. The histological features of group 2a patients resembled hypophosphataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.

The effects of high phosphorus intake on calcium homeostasis.

Survey data confirm that the dietary pattern of many American women who are at high risk of developing osteoporosis is typically high in phosphorus and low in calcium. The imbalance between calcium and phosphorus intake may become more pronounced with continued changes in food preferences and the growing use of phosphorus-containing food additives. Recent studies in young women have shown that a high phosphorus diet moderately low in calcium results in a mild secondary hyperparathyroidism that persists over 4 weeks. Plasma levels of calcitriol did not change despite changes in PTH and serum ionized calcium. Studies on men have shown that dietary phosphorus at levels within the normal range of intakes can affect the renal production and serum concentration of calcitriol. High phosphorus intakes for ten days reduced their plasma calcitriol levels; a 70% reduction in phosphate intake significantly increased their plasma calcitriol. Thus, several lines of evidence indicate that prolonged high phosphorus intake may impair the usual homeostatic mechanisms that come into play when dietary calcium is limited. This, in turn, could impair achievement of maximal bone mass or accelerate bone loss. Although no clinical studies have linked high phosphorus intake with lower bone mass or higher rates of bone loss in humans, this relationship has been demonstrated in animal models. For example, young beagles fed high phosphorus, moderately low calcium diets showed a significant reduction in vertebral bone mass. Current dietary patterns of high phosphorus, low calcium consumption result in persistent changes in calcium regulating hormones that are not conducive to maximizing peak bone mass during growth or slowing the rate of aging bone loss. The net effect of the present dietary pattern on bone status, particularly in teenage and young adult women, needs to be determined. Optimal nutrition early in life, which may include higher calcium and lower phosphorus intakes, together with adequate exercise, may be the most cost-effective approach to the prevention of osteoporotic fractures.

Response of lactating goats to low phosphorus intake 2. Nitrogen transfer from rumen ammonia to rumen microbes and proportion of milk protein derived from microbial amino acids

SummaryFive rumen-cannulated dairy goats were fed diets supplying 2·8 g P/day plus 1·4 g P/kg milk (adequate P) for weeks 1–6 of lactation. Two goats then continued to receive this adequate P supply while three goats were fed deficient diets supplying only 0·8 g P/day plus 0·4 g P/kg milk. Solutions containing CrEDTA and (15NH4)2SO4 were infused into the rumen continuously for 96 h during weeks 5–6 and 11–12, respectively. At intervals following the intraruminal infusion, 15N enrichments of rumen ammonia-N, rumen bacteria-N and milk protein-N were determined. Cr concentration was measured in particle-free rumen fluid.P deficiency did not significantly affect rumen fluid kinetics. It caused a significant increase in pH and reduced the size of the rumen ammonia pool and its outflow rate. Digestibility of organic matter as well as efficiency of microbial protein synthesis were decreased significantly and thus net microbial yield was reduced from 34·1 to 13·7 g N/day. The transfer of N of microbial origin to milk protein decreased from 5·3 to 2·7 g/day, whereas secretion of N in milk protein not originating from rumen microbes remained unchanged at 5·6–5·8 g/day.

Response of lactating goats to low phosphorus intake 1. Milk yield and faecal excretion of P and Ca

SummaryIn weeks 1–6 of lactation, 11 goats were fed diets adequate in phosphorus content, supplying a basal intake of 2·8 g P/day plus 1·4 g P/kg milk produced. In group 1 (three goats), this scheme was continued until week 16. In group 2 (four goats), P supply was changed from an adequate one to a reduced amount by restricting the variable intake to 1·0 g P/kg milk during weeks 7–16 and the basal intake to 0·8 g P/day during weeks 12–16. In group 3 (four goats), P deficiency was caused during weeks 7–11 by a basal intake of 0·8 g P/day plus only 0·4 g P/kg milk. During weeks 12–16 these goats received the same supply of P provided in weeks 1–6.Milk yield was depressed in group 3, but not in group 2. Composition of milk was not affected by P intake in either group. Digestibility of organic matter was reduced from 0·73 to 0·64 by P deficiency treatment. Reduction of faecal P excretion in group 2 appeared to enable P homoeostasis even at the reduced level of P intake. The amounts of P and Ca secreted in milk during P deficiency in group 3 clearly exceeded the corresponding net absorptions. During this period, daily faecal P excretion was reduced to 17 mg/kg live weight. P concentrations in blood plasma, saliva and particle-free rumen fluid were also drastically reduced. Faecal excretion of P increased after the animals returned to the diet supplying adequate P. The increase occurred before the pre-depletion P status had been restored.

Renal aspects of calcium and phosphorus metabolism in preterm infants.

The aim of this study is to emphasize renal aspects of calcium and phosphorus metabolism from our data of more than 200 metabolic balance studies carried out in preterm infants. Renal production of 1,25-dihydroxyvitamin D increased rapidly after birth provided the concentration of the substrate, 25-hydroxyvitamin D, is adequate. The gut of preterm infants is able to respond to the active metabolite of vitamin D. Mean plasma phosphate threshold for tubular reabsorption of phosphate is high, about 2.1 mmol/l or 6.5 mg/dl. The low fractional excretion of phosphate cannot be explained by immature parathyroid function nor by renal unresponsiveness to parathormone, at least after the first days of life. It is probably due to regulating factors related to the high rate of growth. Because of reduced glomerular filtration rate, a too high phosphorus intake may result in hyperphosphatemia. Conversely, a too low phosphorus intake will lead to a phosphate depletion syndrome characterized by marked increase in urinary calcium excretion, no urinary phosphate, and hypophosphatemia. Preterm infants with chronic metabolic acidosis are able to acidify urine so that titratable acid is directly related to urinary excretion of phosphate. Clinical implications are that calcium:phosphorus ratio in milk must be adapted according to net bone and soft tissue retention.

Biological characteristics for assessing low phosphorus intake in finishing swine.

Three replicates of a randomized complete-block design in a 3 x 3 factorial arrangement of treatments involving 141 pigs were conducted to evaluate the effect of low P intake on various response criteria in swine from 65 to 95 kg body weight. Total dietary P levels of .09, .21 and .31% were each fed in a Ca:P ratio of 1.1, 1.5:1 or 2:1 for a 35-d experimental period. The basal diet was formulated using corn starch, dextrin and a soy protein concentrate with monosodium phosphate and limestone supplying desired treatment levels of Ca and P. Blood and bones were collected for mineral analysis. Gain and feed performance responses were not affected by Ca:P ration or dietary P level for the 35-d period. Serum inorganic P concentrations declined as Ca:P ratio increased, but increased as dietary P increased. Serum alkaline phosphatase activity increased with higher Ca:P ratios, and decreased as dietary P level increased. Percent bone ash was not influenced by Ca:P ratio, but increased as dietary P level increased. Bone-bending moment was influenced by Ca:P ratio, and increased linearly as dietary P increased. Dietary P level resulted in a linear increase in total bone and its ash component weight, and in the accretion of the ash and organic matrix component. These data suggest that between 65 to 95 kg body weight, percent bone ash was affected by dietary P level, while bone-bending moment, bone component weights, their accretion, both dietary p level and Ca:P ratio.

Biological characteristics for assessing low phosphorus intake in growing swine.

A total of 195 swine from 18 to 35 kg were used to evaluate various biological responses of growing swine fed low P diets at different Ca:P ratios. Three replicates of a randomized complete-block design in a 3 X 3 factorial arrangement of treatments were used. Total dietary P levels of .12, .31 and .50% were fed in 1:1, 1.5:1 or 3:1 Ca:P ratios. Diets were formulated using corn starch, dextrin and soy protein concentrate, with monosodium phosphate and limestone used to supply appropriate dietary treatment levels of Ca and P. Gain and feed performance were generally influenced by both Ca:P ratio and dietary P level. Serum inorganic P decreased linearly as Ca:P ratio widened and increased linearly as dietary P increased. Serum Ca concentrations responded inversely to serum inorganic P in response to both Ca:P ratio and dietary P level. Serum alkaline phosphatase was not affected by Ca:P ratio, but declined quadratically with increasing dietary P level. Bone bending moment was influenced by both dietary P level and Ca:P ratio. Bone component weights (ash, organic matrix), percentage bone ash and net accretion of bone ash and organic component weights were not influenced by Ca:P ratio but increased linearly as dietary P level increased. These results suggest that bone component weights, net ash accretion and percentage bone ash were more sensitive criteria than bone bending moment or serum alkaline phosphatase, which in turn were more sensitive than serum inorganic P, Ca, Mg and growth performance characteristics in response to dietary P level.

An evaluation of various biological characteristics in assessing low phosphorus intake in weanling swine.

A total of 204 weanling pigs were utilized in an experiment of 3 X 3 factorial design (in three replicates) to evaluate the effects of feeding low P diets for a 35 d period on various growth, serum and bone measurement characteristics. Total dietary P levels of .23, .35 and .55% were fed in a Ca:P ratio of 1:1, 1.5:1 or 3:1. The basal diet was formulated using cornstarch, dextrin and soy protein concentrate with monosodium phosphate and limestone used to supply appropriate dietary levels of Ca and P. Growth, serum minerals and serum alkaline phosphatase were evaluated at 21 and 35 d of the trial. At the end of the experiment six pigs/treatment group were killed and bones were collected for various measurement criteria. Daily gain, feed intake and feed conversion were not affected by Ca:P ratio, but there was an increased gain and feed intake response to dietary P level. Serum inorganic P decreased with increasing dietary Ca:P ratio and also increased linearly as dietary P level increased. Serum alkaline phosphatase activity was not influenced by dietary Ca:P ratio, but did decrease as dietary P level increased. Bone bending moment increased quadratically as Ca:P ratio increased, but also increased linearly with dietary P level. Percentage bone ash, bone ash and organic matrix weights and the accretion of both the mineral and matrix components were not affected by Ca:P ratio, but each was influenced as dietary P increased. These data suggest that percentage bone ash, bone component weights and accretion measurement characteristics were more sensitive indicators of dietary P levels than bone bending moment, serum alkaline phosphatase and serum P, which in turn were superior to serum Ca, Mg and growth performance.

Effect of phosphorus intake on growth rate, food intake and quality of the skeleton of growing lambs infected with the intestinal nematode Trichostrongylus vitrinus

The performance of growing lambs dosed daily for 12 weeks with 2500 Trichostrongylus vitrinus larvae (I) or given no larvae (control, C) was compared at two levels of phosphorus intake; 2.75 gP/kg dry matter (normal, NP) and 1.88 pgP/kg dry matter (low, LP). Both low phosphorus and T vitrinus infection reduced dry matter intake and growth rate and the combined effect of low phosphorus and infection were additive. Plasma hypophosphataemia (less than 60 mg per litre) occurred in groups CLP, ILP and INP from week 3, the values gradually returning to normal levels in INP lambs by the end of the trial. T vitrinus infection did not depress plasma phosphorus concentration below that seen in the low phosphorus controls. Both low phosphorus intake and T vitrinus infection reduced the density and mineralisation of bone, the most severely affected bones occurring in groups ILP lambs. T vitrinus infection reduced the content and concentration of phosphorus in the rumen and the effect was greater at the lower intake of phosphorus. Infection also reduced the proportion of phosphorus in the rumen liquid phase. The number of T vitrinus recovered from the intestine was higher and villous atrophy more extensive in lambs from group ILP. It is suggested that development of 'resistance' may be delayed on a low phosphorus intake.

Calcium and phosphorus economy of the preterm infant and its interaction with vitamin D and its metabolites.

Senterre, J. and Salle, B. (Departments of Neonatology, University hospital, Liège, Belgium and Lyon, France). Calcium and phosphorus economy of the preterm infant and its interaction with vitamin D and its metabolites. Acta Paediatr Scand, Suppl. 296: 85, 1982.—One hundred and seventeen 3‐day metabolic balance studies were carried out in 69 preterm infants. Matched groups of infants were fed either banked human milk, an infant formula or a low birthweight infant formula with medium‐chain triglycerides. In addition groups were constituted according to the vitamin D intake or the administration of 1,25–dihydroxyvitamin D. In infants fed human milk, mean fat absorption was 77%. Calcium absorption was 49±11% with no vitamin D supplementation and it reached 70±11% with a daily oral dose of 30 g of vitamin D. However in this latter group urinary excretion of calcium was very high because of the low phosphorus intake. With infant formula, mean fat absorption was 73%. Calcium absorption was 20±11% with no vitamin D supplementation, 32±13% with 25 g of vitamin D per day and 49±10% with daily administration of 0.5 g of 1,25‐dihydroxyvitamin D. With low birthweight infant formula, mean fat absorption was 90%. Calcium absorption was 32±15% with no vitamin D supplementation, 45±13% with 25 g of vitamin D, 59±10% with 50 g of vitamin D and 58±6% with 0.5 g of 1,25‐dihydroxyvitamin D per day. However with this active metabolite of vitamin D, serum level and urinary excretion of calcium were significantly higher. Whatever the milk or the vitamin D intake, phosphorus absorption was about 90%. Phosphorus retention was related to nitrogen plus calcium retentions. This study indicates that vitamin D status is the major factor regulating intestinal absorption of calcium. Activation pathways of vitamin D and gut response to 1,25‐dihydroxyvitamin D are operative in preterm infant. However in populations where relative vitamin D deficiency is common as in the present study, it seems necessary to give preterm infants a daily oral dose of 30 to 50 g (1200–2000 IU) of vitamin D for achieving maximal calcium absorption. Preferably, plasma 25‐hydroxyvitamin D level should guide the clinician in estimating the sufficiency of vitamin D intake.

Calcium and Phosphorus Supplementation of Rations for Lactating Cows

Forty Holstein cows were assigned among four dietary treatments that resulted in dietary calcium and phosphorus: 1) 1.0%, .31%; 2) 1.0%, .54%; 3) 1.8%, .30%; and 4) 1.7%, .54%. Calcium was supplemented as ground limestone and phosphorus as sodium tripolyphosphate. Treatment diets were fed from parturition until 10 mo postpartum. Cows fed diets low in phosphorus had lower milk yields, feed intakes, and poorer efficiencies of milk production. Inorganic phosphorus in blood plasma was reduced by low phosphorus intake. Overall, calcium of the diet did not affect milk production. However, there was a significant calcium-phosphorus interaction with increased milk production and greater feed intake when calcium was added to low phosphorus diets but not to diets containing excess phosphorus. Added calcium did not affect inorganic phosphorus, calcium, or magnesium of blood plasma. Fecal pH was increased and percent starch in the feces decreased with added dietary limestone. Efficiency of milk production was not improved by added limestone. Maximum milk yields and performance cannot be obtained with .3% dietary phosphorus.

Urinary Calcium and Calcium Balance in Young Men as Affected by Level of Protein and Phosphorus Intake

Eight young adult males were subjects in a 51-day metabolic study conducted to examine the effects of level of protein and of phosphorus intake on urinary calcium and calcium balance. Two levels of protein (50–150 g) were given at each of two levels of phosphorus intake (1,010 and 2,525 mg). Dietary calcium and magnesium were maintained at 500 and 350 mg, respectively. Raising the protein intake from 50 to 150 g caused a calciuresis at both phosphorus intakes, but the actual increase in urinary calcium was 71 mg/day greater at the low than at the high phosphorus intake and calcium balance was changed from 24 to -116 mg/day at the low phosphorus intake and from 8 to -25 mg/day at the high. When the phosphorus intake was raised, urinary calcium decreased from 156 to 93 mg/day at the low protein intake and from 334 to 200 mg/day at the high protein intake and the markedly negative calcium balance found at the high protein intake was greatly improved. Simultaneous increases in protein and phosphorus intakes caused a 28% increase in urinary calcium whereas the increase in protein intake alone caused a 115% increase.protein phosphorus calcium balance

Low phosphorus intake and vitamin D metabolism and expression in rats.

Male weanling rats, depleted of vitamin D for 4 wks., were repleted for 4 wks. with 1,2 — [3H]-4-[14C]-vitamin D3 and then placed on three regimens: normal mineral intake (0.4% Ca, 0.3% P); low-Ca (0.004% Ca, 0.3% P) and low-P (0.4% Ca, 0.13% P). Three weeks later 1,25-dihydroxyvitamin D3 (1,25-(OH)2-D3) levels were determined in plasma and intestine on the basis of the 3H/14C radioactivity ratios. Calcium-binding protein (CaBP) was estimated in parallel experiments with 4 groups of rats that had been on semi-synthetic regimens containing 1.5% Ca, 1.5% P; 1.5% Ca, 0.2% P; 0.06% Ca, 0.2% P; and 1.5% Ca, 0.03% P for 7–10 days. In comparison with the controls, the low Ca diets Zed to a doubling in 1,25-(OH)2-D3 levels in intestinal mucosa, and to detectable levels of 1,25-(OH)2-D3 in plasma. CaBP was markedly elevated. On the other hand, in the low P groups, in spite of hypophosphatemia, 1,25-(OH)2-D3 was undetectable in plasma and virtually undetectable in intestine. Moreover, CaBP levels were unchanged on 0.2% P intakes and markedly depressed on 0.03% P. Hypophosphatemia became more pronounced as P intake decreased, while plasma Ca increased. It therefore appears that in rats, as contrasted with chickens, hypophosphatemis is not a major factor regulating metabolism and expression of 1,25-(OH)2-D3.

Effect of phosphorus on the 90Sr balance in man.

The effect of a high phosphorus intake on the excretion and retention of 90Sr in man was studied by determining 90Sr balances. The phosphorus intake averaged 800 mg/day in the control study and 2000 mg/day in the experimental study. As the effect of phosphorus on 90Sr metabolism may be influenced by the intake of calcium, the studies were carried out during both a low calcium intake of 200 mg/day and a high calcium intake of 2000 mg/day. In the control study, during a low calcium intake of 200 mg/day, a phosphorus intake of 800 mg/day, and a dietary 90Sr intake of about 5 pCi/day, the 90Sr balance averaged +0.2 ± 0.5 pCi/day. Raising the phosphorus intake to 2000 mg/day during the low calcium intake had little effect on the 90Sr balance, which changed from +0.2±0.5 to −0.1±0.5 pCi/day. During a high calcium intake of 2000mg/day and a low phosphorus intake of 800 mg/day, the 90Sr balance averaged −0.7 ± 0.4 pCi/day. Increasing the phosphorus intake to 2000 mg/day during this high calcium intake resulted in further negativity of 90Sr balance, which averaged −1.3 ± 0.2 pCi/day. These studies have shown that the addition of phosphorus to a low calcium intake of 200 mg/day did not affect the 90Sr balance, while the addition of phosphorus to a high calcium intake resulted in a negative 90Sr balance.

Bicarbonate-induced phosphaturia: Dependence upon the magnitude of phosphate reabsorption.

The acute effect of bicarbonate infusion on inorganic phsophate (Pi) reabsorption was determined in thyroparathyroidectomized (TPTX) rats stabilized on a high phsophorus diet. In the normophosphatemic state, bicarbonate did not affect Pi reabsorption significantly. On the other hand, after hyperphosphatemia was induced by phosphate loading, bicarbonate inhibited Pi reabsorption. In order to determin if eht aboslute level of plasma or filtered Pi was an improtant determinant of this phosphaturic action of bicarbonate during hyperphosphatemia, equivalent rates of Pi reabsorption were achieved after phosphate infusion in TPTX rats previously stabilized on a low dietary phosphorus intake, but at significantly lower plasma Pi concentrations and filtered Pi loads than in their high dietary phosphorus counterparts. Bicarbonate inhibited Pi reabsorption equivalently in both hyperphosphatemic groups, indicating that the magnitude of Pi transport itself was of importance in determining the inhibitory response to bicarbonate. In addition, the results suggest that transport mechanisms for bicarbonate and Pi may interact competitively.

Differences in duodenal calcium-binding protein (CaBP) in response to a low-calcium or a low-phosphorus intake

In the chick, changes in the amount of intestinal calcium-binding protein can be produced by restriction of either dietary calcium or dietary phosphorus [6]. Intestinal adaptation to a low-calcium intake is modulated by regulation of la,2Sdihydroxycholecalciferol (la,25-DHCC) synthesis in the kidney, whereas at least part of the intestinal response to a low-phosphorus diet seems to be independent of changes in the hydroxylation of vitamin D in the kidney [1]. Furthermore some studies [2, 7] suggest that, in the rat, the modulation of active calcium transport by dietary phosphorus involves other factors in addition to the stimulation of la,25DHCC synthesis. The purpose of the present report was to determine whether or not the modulation of CaBP produced by calcium and phosphorus restriction in the rat results only from increased la,25-DHCC production. CaBP adaptation to calcium and phosphorus restriction was studied in rats either fed ad lib. or pair-fed in terms of vitamin D deficiency, la,25-DHCC administration, and vitamin D 3 intake.

Control of calcium absorption and intestinal calcium-binding protein synthesis

A current hypothesis suggests that the degree of Ca absorption is hormonally controlled via the feed-back regulation of 1,25-dihydroxycholecalciferol (1,25-(OH) 2D 3) production from 25-hydroxycholecalciferol (25-OHD 3) by kidney 1-hydroxylase. To test this hypothesis, dihydrotachysterol 3 (DHT 3), a steroid not requiring 1-hydroxylation for biological activity, was given to chicks as the only source of vitamin D-activity. As expected, DHT 3-treated chicks did not adapt to a calcium-deficient diet. However, both the efficiency of Ca absorption and net synthesis of CaBP were stimulated in DHT 3-treated chicks by a low phosphorus intake, providing evidence for an alternate pathway of control.

Rarity of renal osteodystrophy in Israel due to low phosphorus intake. A natural experiment.

Renal osteodystrophy is very rare in undialysed chronic renal failure in Israel, and common in Western Europe and North America. In a dietary survey it was found that there was a lower dietary phospho

A METHOD FOR THE URETERAL CATHETERIZATION AND THE DETERMINATION OF THE GLOMERULAR FILTRATION RATE IN RATS; WITH SOME APPLICATIONS ON THE STUDY OF PARATHYROIDS

Fine polyethylene tubes were inserted in the ureters of female rats under nembutal anesthesia. Several hrs. later, the rats were injected intravenously with creatinine. Every 5 mins. urine was collected for 30mins. following the injection then the animals were sacrificed. A linear line was obtained when the rate of creatinine excretion was plotted on a logarithmic scale against time, and the rate of creatinine excretion at the time of sacrifice was obtained by extrapolation. Creatinine clearance was 1.94ml/min. or 0.87ml/min./100g body weight. No difference was found in creatinine clearance of rats between low phosphorus diet and control normal diet groups. Parathyroidectomy caused only a slight and statistically insignificant decrease in creatinine clearance. Renal net reabsorption of phosphorus increased by 26% after low phosphorus intake and 48% after parathyroidectomy. The result supports the view that the parathyroids have an influence on renal tubules.