Phosphate Excretion Rates Research Articles

Effect of parathyroid hormone on renin secretion.

The ability of parathyroid hormone (PTH) to increase renin secretion was investigated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH 1-34, at the dose of 0.028 microgram/kg-1 min-1 increased renin secretion by 149% (501 +/- 105 to 1249 +/- 309 ng hr-1 min-1); renin secretion returned to control values during the recovery period. In order to determine whether PTH acted directly on the kidney to increase renin secretion, PTH was infused into the right renal artery at doses of 0.0014 to 0.0028 microgram/kg-1 min-1 and renin secretion from the right kidney was compared to that from the left (control) kidney. Renin secretion from the right (PTH-infused) kidney was not greater than control values for that kidney or different from the renin secretory rate of the left (control) kidney. In contrast, the excretion rates of both phosphate and sodium from the right kidney were greater than control values and from the excretion rates of the left kidney. These data suggest that PTH, while acting directly on the kidney to increase phosphate and sodium excretion, does not elevate renin secretion by a direct renal action.

Tubular capacity of phosphate transport in phosphate-deprived rats: effects of nicotinamide and PTH.

The present study tested the hypothesis that nicotinamide and/or parathyroid hormone (PTH) would reverse the resistance of phosphate-deprived rats to the phosphaturic effects of phosphate infusions by reducing the tubular capacity for phosphate transport. The response to progressively increasing rates of phosphate infusion (1, 2, and 3 mumol/min) was evaluated in thyroparathyroidectomized (TPTX) rats fed low phosphate diet (0.07%) for 4 days and treated with either vehicle or nicotinamide 2 h before the experiment. Following phosphate infusions, phosphate excretion was unchanged in vehicle-treated rats but increased progressively in nicotinamide-treated rats to 60% of the final rate of infusion. In a second series conducted in the presence of exogenous PTH, vehicle-treated rats responded to phosphate infusions by increasing phosphate excretion to 80-90% of the rate of infusion. In the presence of both nicotinamide and PTH, the rate of phosphate excretion matched the rate of infusion. Vehicle-treated rats displayed the highest reabsorptive rates without reaching a transport maximum, whereas a lower maximum reabsorptive rate was evident in nicotinamide-treated rats. However, in both groups given PTH, not only was the transport maximum lower but it declined with further increases in filtered load. We conclude that nicotinamide and PTH reverse the effects of dietary phosphate deprivation by decreasing the tubular capacity for phosphate transport.

Dysfunction of tubular phosphate reabsorption related to glomerular filtration and blood glucose control in diabetic children.

The renal handling of inorganic phosphate was studied by measuring the urinary excretion rate of phosphate (UPO4V), phosphate-(Cr51) EDTA clearance ratio (CPO4/GFR) and maximal tubular reabsorption of phosphate per litre glomerular filtrate (TmPO4/GFR) during fasting in 26 ambulatory Type 1 (insulin-dependent) diabetic children without clinical signs of microangiopathy (age: 7-14 years; duration of disease: 3-14 years). Similar measurements were made in 28 healthy schoolchildren (age: 8-14 years). UPO4 V and CPO4/GFR were significantly enhanced in the diabetic children (p less than 0.001) and correlated with the degree of hyperglycaemia (p less than 0.005). TmPO4/GFR was significantly suppressed in the diabetic children (1.23 versus 1.73 mmol/l, p less than 0.001). This disturbance was neither related to changes in serum parathyroid hormone nor to growth hormone concentrations but was inversely correlated with the degree of hyperglycaemia (r = -0.61, p less than 0.001) and with tubular reabsorption of glucose (r = -0.53, p less than 0.01). In spite of the markedly lowered TmPO4/GFR in the diabetic subjects, the mean maximal (TmPO4) and absolute tubular phosphate reabsorption rates were equal to those of the 28 healthy subjects. Both in the diabetic and healthy subjects, these parameters were positively correlated with glomerular filtration rate which was significantly elevated in the diabetic children (138 versus 109 ml/min per 1.73 m2, p less than 0.01). The study demonstrates a dysfunction in tubular phosphate reabsorption in diabetic children which is related to glycaemic regulation.

Oxygen consumption and ammonia and phosphate excretion in pond zooplankton

Respiration and ammonia and phosphate excretion were studied in the temperature‐acclimated zooplankton of a small eutrophic fishpond. The zooplankton included species of Cyclopoida, Cladocera, and Rotatoria. Their body size varied from ng to µg of protein nitrogen. Oxygen consumption was linearly related to body size at 11°C or higher, but proportional to the 0.86 power of size at 4°C. Similar size relationships applied for N and P excretion. Relationship of oxygen uptake to temperature was virtually identical in well fed Cyclops vicinus and Daphnia hyalina.The oxygen equivalent of ammonia excretion for protein catabolism was never higher than the measured oxygen consumption; there was no suggestion of an apparent gluconeogenesis or lipogenesis in well fed Cyclops. Relative excretion rates of ammonia and phosphate were related to feeding level. The lowest rates of ammonia excretion were at low natural levels of feeding while they increased both in fasting and well fed animals. Relative phosphate excretion rates increased with increasing food concentration, but individual experiments were not comparable. Herbivorous pond plankton had lower N‐excretion rates than carnivorous, which is comparable with planktophagous fish rates published previously.

The influence of continuous intragastric feeding of liquid food (Vivonex) on the diurnal excretion of electrolytes and urea in rats

Abstract The diurnal excretion patterns of several electrolytes and urea were studied in 5 freely moving rats on an elemental diet (Vivonex) administered either orally or as a continuous intragastric feeding; the lights were on from 07.00–19.00 h and off from 19.00–07.00 h. During continuous feeding the diurnal rhythms persisted, although the amplitude was lower than during oral feeding. The maximum excretion rates of potassium, phosphate and urea all coincided under both feeding regimens. The time of the maximum calcium excretion rate coincided with that of sodium during oral feeding but not during continuous feeding. During continuous feeding the maximum calcium excretion rate shifted from 04.00 to 10.00 h. The diurnal excretion of magnesium during continuous feeding was abolished, possibly as a result of the low calcium intake. From this study it can be concluded that duringcontinuous intragastric feeding all of the studied excretion patterns persist, with the exception of magnesium, which indicates that these rhythms are not merely the result of the intermittent intake of food and minerals.

Ammonia and Inorganic phosphate excretion by zooplankton from inshore waters of the Great Barrier Reef, Queensland. I. Relationship between excretion rates and body size

Ammonia and phosphate excretion rates were measured on various copepods and some ctenophores, siphonophores, decapod larvae, mollusc larvae, polychaete larvae, chaetognaths and appendicularians from inshore waters of the Great Barrier Reef during warm and cold seasons. Regression analyses showed high correlations between the excretion rate and body weight of zooplankton: in the warm season, log yn = 0.518 + 0.525 log x (n = 348. r = 0.612) log yp = -0.174 + 0.429 log x (n=117, r=0.570), and in the cold season, log yn = 0.186 + 0.518 log x (n = 268, r = 0,777) log yp = -1.002 + 0.740 log x (n = 255, r = 0.694), where yn is ammonia excretion (nanograms N per animal per hour), yp is phosphate excretion (nanograms P per animal per hour), x is body dry weight (micrograms per animal); n is the number of measurements, and r is the correlation coefficient. Since the two regression lines for ammonia excretion were parallel a Q10 value of 2.53 was calculated from the results of warm and cold seasons. This calculation was not possible for the phosphate excretion because the regression lines between the seasons were not parallel. The mean ratio of ammonia excretion to phosphate excretion (N:P ratio, by atoms) was 28.56 in the warm season and 24.48 in the cold season. The present results were compared with those of other workers who used zooplankton from different seas, and the effects of experimental conditions, such as injury of specimens, container size, incubation time and feeding on the excretion rates are discussed.

Increased serum 1,25-(OH)2-vitamin D concentrations fail to affect serum or urine phosphate in humans.

Patients with recurrent calcium oxalate/apatite nephrolithiasis in association with hypercalciuria (idiopathic hypercalciuria) may exhibit low serum inorganic phosphate concentrations (1,2,3,4) in association with normal rates of urinary phosphate excretion implying the existence of impaired renal tubular phosphate reabsorption. In fact, such calcium stone formers exhibit impaired renal phosphate conservation in response to ingestion of a diet low in phosphate (5). They also exhibit higher than normal salivary phosphate concentrations (6) implying the presence of a more generalized abnormality of phosphate transport. Dietary phosphate deprivation in animals is accompanied by increased synthesis of the calcium mobilizing steroid 1,25-(OH)2-vitamin D3 by the kidney (7) and elevated serum levels of this hormone (8). Similarly renal synthesis of 1,25-(OH)2-D is increased in hypercalciuric kidney stone formers (9) and high serum 1,25-(OH)2-D concentrations among these patients may be inversely related to the degree of hypophosphatemia (4).KeywordsIdiopathic HypercalciuriaDietary PhosphateUrinary Phosphate ExcretionSerum Inorganic Phosphate ConcentrationDietary Phosphate IntakeThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Short-term starvation effects on nitrogen and phosphorus excretion by the chaetognath Sagitta enflata

Freshly captured Sagitta enflata exhibited specific excretion rates of ammonium and phosphate (expressed as percentage body content of N or P per hour) that were not significantly related to the size of individual animals. The degree of crowding in experimental vessels was positively correlated with specific excretion rates of ammonium. Excretion rates, under conditions that precluded feeding, decreased sharply during the first several hours' incubation time, approaching the rates exhibited by animals starved overnight. The practice of holding freshly captured zooplankton for a time before determining excretion rates may seriously affect those rates, if the animals are unable to feed. Animals captured during the day in Kaneohe Bay, Hawaii, having no food items in their guts, had mean specific excretion rates (±s.d.) of 0·81±0·51% body content of N h−1 for ammonium, and 1·29±1·24% body content of P h−1 for phosphate. Minimal estimates of natural excretion rates, made from the first hour of incubation in further experiments, were 1·19±0·47% h−1 for nitrogen and 3·8±3·95% h−1 for phosphorus. Sagitta is not a large contributor to nutrient regeneration in Kaneohe Bay.

Urinary excretion of cyclic nucleotides and phosphate in response to parathyroid hormone and calcitonin in man.

The response to parathyroid hormone (PTH) and calcitonin (CT) was studied in eight children with various bone diseases by determining the serum calcium (Ca) and phosphate (P) concentration, urinary phosphate excretion rate, renal phosphate clearance, the percentage of filtered phosphate reabsorbed by the renal tubule (%TRP), creatinine clearance (Ccr), urinary cyclic adenosine 3',5' monophosphate excretion rate (UcGMPV). Administration of PTH caused no significant change in serum Ca and P values, whereas CT produced a decrease in Ca (delta Ca, -1.4 +/- 0.1 mg/100 ml) and P (delta P; -1.1 +/- 0.1 mg/100 ml). There was an increase in UcAMP V (delta UcAMP; 437 +/- 74 nmoles/min/100 ml Ccr) without any significant change in UcGMPV after administration of PTH. Phosphaturia was produced by both PTH (delta TRP, -18 +/- 3%) and CT (delta TRP, -13 +/- 2%). However, CT did not elicit any increase in either UcAMPV or UcGMPV.

Utilization and metabolic effects of a conventional and a single-solution regimen in postoperative total parenteral nutrition

A comparison was made of the effects of two intravenous regimens for postoperative total parenteral nutrition, namely, a conventional (control) regimen (group I) and a single-solution regimen of the same composition (group II). The effects examined were: hemoglobin concentration, prothrombin time, serum protein and electrolyte concentrations, and nitrogen and electrolyte balances. The 18 patients undergoing abdominal surgery were allocated at random to the two groups and the experiment was run for 3 days. During the day of the operation and the next 3 days both groups showed a decrease in the hemoglobin concentration and in the serum levels of iron, albumin, transferrin and cholesterol, while the asparagine aminotransferase increased. During total parenteral nutrition the prothrombin time and erythrocyte sedimentation rate increased in both groups. The nitrogen balance improved gradually in both groups and on the 3rd day was positive in group II. The calcium and magnesium balances indicated a higher retention and the phosphate balance a lower retention of these ions in group II than in group I. The urinary phosphate excretion rate during total parenteral nutrition decreased in both groups. This study indicates that the single-solution regimens used in intravenous nutrition caused no adverse metabolic effects and was used as efficiently as a conventional regimen in the early postoperative period.

Acute effect of high dose (48 mg) of piretanide in advanced renal insufficiency.

1 The acute effects of a high dose of piretanide, a new potent diuretic were studied in eight patients with severely impaired renal function (GFR between 0.09 and 0.17 ml s-1 1.73 m-2). 2 After hydration and following two control periods, a single dose of 48 mg piretanide was ingested. Thereafter, urine was collected every 30 min for 2 h and every hour for the next 4 h. Urinary fluid losses were replaced orally (100 ml of water ever hour) and intravenously (isotonic saline + glucose infusion). 3 The following measurements were made: urine flow rate, clearances of inulin, PAH, urea, creatinine, uric acid, osmolar and free water clearances, excretion rates of sodium, chloride, potassium, calcium, phosphate, bicarbonate, ammonium, titratable acidity and urine pH. 4 Piretanide (48 mg) appeared to be effective in advanced renal insufficiency, producing a significant increase in urine flow rate, in sodium, chloride, potassium and calcium excretion and in Cosm. 5 There was no significant change in GFR, as measured by inulin clearance, or in the other measured parameters.

Activity of a new high efficiency diuretic in man: piretanide (HOE 118).

1 The pharmacological actions of piretanide, a new high efficiency diuretic, were studied in sixteen patients with GFR (inulin clearance) varying from 0.1--2.5 ml/s. 2 After hydration and following two control periods, a single dose of 6 mg piretanide was ingested. Thereafter, urine was collected every 30 min for 2 h and every hour for the next 4 h. Fluid losses were replaced. 3 The following measurements were made: urine flow rate, clearances of inulin, PAH, urea, creatinine, uric acid, osmolar and free water clearances, excretion rates of sodium, chloride, potassium, calcium, phosphate, bicarbonate, ammonium, titratable acidity and urine pH. 4 Main results showed piretanide was efficient in the group with normal GFR (inulin clearance greater than 1.5 ml/s) and in the group with slightly decreased GFR (1.0 less than inulin clearance less than 1.4 ml/s), in terms of diuresis, natriuresis, kaliuresis and calciuresis. It was inefficient in the group with severe renal insufficiency (inulin clearance less than 0.3 ml/s). 5 Free water clearance showed preservation of diluting ability to a large extent. 6 In the three groups, no significant change in inulin clearance and PAH clearance occurred.

Mechanism of the phosphaturia due to chlorothiazide.

CTZ caused a phosphaturia when baseline phosphate excretion was not already high. Furthermore, when th influence of PTH is withdrawn, the excretion of phosphate appears to be largely affected by changes in urinary pH.

1 Endocrine manifestations of systemic disease

1 Endocrine manifestations of systemic disease

The urine cyclic AMP response to parathyroid extract (PTE) administration in normal subjects and patients with parathyroid dysfunction

Fourteen normal subjects, 21 patients with primary hyperparathyroidism, and 12 patients with hypoparathyroidism were studied to evaluate the effects of an excess or deficiency of endogenous parathyroid hormone (PTH) and of serum calcium and phosphate upon urinary cyclic AMP and phosphate responses to PTE administration in man. Preoperatively, the hyperparathyroid patients were hypercalcemic and hypo- or normophosphatemic; post-operatively, they were hypo- or eucalcemic and euphosphatemic. The hypoparathyroid patients were hypocalcemic and hyperphosphatemic. Hourly urine specimens were collected from 8:00 a.m. to 12:00 noon on two consecutive days and analyzed for their cyclic AMP, phosphate, and creatinine contents. On the second day, 200 USP units of PTE were administered intravenously over a period of 5 min beginning at 9:00 a.m. Cyclic AMP excretion in the control period, prior to PTE infusion, was significantly elevated in the hyperparathyroid patients preoperatively, but fell to normal postoperatively, and was significantly depressed in the hypoparathyroid patients. Phosphate excretion during the same control period was significantly elevated to near maximal levels in the hyperparathyroid patients preoperatively, but fell to normal postoperatively and was not significantly different from normal in the hypoparathyroid patients. Following PTE administration, the same maximal levels of cyclic AMP and phosphate excretions were observed in all of the groups studied. Thus, there were no apparent effects of endogenous PTH levels or serum calcium and phosphate levels on the maximum excretion rates of cyclic AMP or phosphate following PTE administration in patients with hyper- or hypoparathyroidism.

Evidence for a renal PO4 leak in patients with calcium nephrolithiasis.

Patients having recurrent calcium oxalate and/or apatite nephrolithiasis demonstrate hypophosphatemia but normal rates of glomerular filtration and urinary phosphate excretion in comparison to healthy adults without a personal or family history of renal stones. These observations suggest that stone formers have a defect in net renal tubular reabsorption of filtered PO4. We compared the responses of stone formers and of normal subjects to dietary PO4 deprivation in order to assess whether the lower serum PO4 levels in stone formers are the result of a renal PO4 leak or a resetting of the level at which the kidneys regulate serum PO4 levels. Nine male stone formers and 13 healthy male adults were studied while eating normal diets and then while eating a liquid diet providing only 2 mmol PO4/day for 3 days. (Females were not studied because serum PO4 falls in healthy women deprived of dietary PO4.) During control, serum PO4 averaged 1.30 ± 0.06 SE mmol/L in normals and 1.28 ± 0.06 mmol/L in stone formers, values that are not different for these small groups. Control UPO4V averaged 32.4 ± 1.8 mmol/day in normals and 27.9 ± 2.3 mmol/day in the stone formers. These means are also not significantly different. However, after 3 days of dietary phosphate deprivation, mean serum PO4 concentrations declined by −0.18 ± 0.04 mmol/L in stone formers (p < 0.01) but did not change from control in the normal men (+0.05 ± 0.05 mmol/L; NS). The mean change from control in serum PO4 concentrations in stone formers was also significantly different from the change in normals (p < 0.01). In addition, UPO4V on the 3rd day of dietary PO4 deprivation fell to only 4.5 ± 1.0 mmol/day in stone formers, a value significantly higher than that observed in the normal men of 1.8 ± 0.5 mmol/day (p < 0.02). The observations that stone formers fail to achieve normal maximum renal PO4 conservation and demonstrate a fall in serum PO4 concentration in response to dietary PO4 deprivation provides further support for the view that these patients have a renal PO4 leak. The mechanism of such a leak remains to be determined. The suppression of PTH secretion that accompanies dietary PO4 deprivation in normal subjects could be impaired or delayed among stone formers. Alternatively, stone formers may have a defect in a PTH-independent renal tubular PO4 transport process.

Lack of dependence of urine PCO2 upon reduction of glomerular filtration rate in alkalotic dogs.

1. The PCO2 gradient between alkaline urine and arterial blood (U-B PCO2) is thought to depend primarily on distal hydrogen ion secretion. However, other variables affecting the U-B PCO2 include the urine flow rate, the urinary bicarbonate and phosphate excretion rates and the glomerular filtration rate. 2. In order to evaluate the effects of acute changes in these factors on the U-B PCO2, bicarbonate-loaded dogs with maximal U-B PCO2 values were subjected to either acute unilateral elevations of ureteral pressure or hypotension caused by nitroprusside infusion. The results demonstrate that acute reduction in the glomerular filtration rate does not cause a decrease in the U-B PCO2 as long as the urinary concentrations of phosphate and bicarbonate do not decline. 3. Urinary concentrations of phosphate and bicarbonate appeared more important than their excretion rates in the maintenance of elevated U-B PCO2 values.

The effect of laboratory conditions on the extrapolation of experimental measurements to the ecology of marine zooplankton. IV. Changes in respiration and excretion rates of boreal zooplankton species maintained under fed and starved conditions

Herbivorous zooplankton species (Calanus plumchrus, Paracalanus parvus and Euphausia pacifica) and carnivorous species (Parathemisto pacifica and Pleurobrachia pileus) collected from Saanich Inlet, British Columbia, Canada, were maintained in the laboratory under fed and starved conditions. Respiration rate and excretion rates of ammonia and inorganic phosphate were measured successively on the same batch populations of each species in different feeding conditions. Respiration rate remained at a constant level or increased during the feeding experiment but decreased progressively in starved individuals. Herbivorous, but not carnivorous, species showed a rapid decrease in both excretion rates for the first few days of an experiment irrespective of feeding conditions. However, the general level of excretion rates of fed specimens was higher than that of starved ones. The O:N, N:P and O:P ratios were calculated from respiration, ammonia excretion and phosphate excretion and discussed in relation to metabolic substrates of animals during the experiment. A marked difference was shown in the O:N ratio between fed hervivores (>16) and fed carnivores (7 to 19), suggesting highly protein-oriented metabolism in the latter. One unknown factor causing variation in excretion rates is speculated to be the physiological stress on animals during sampling from the field. It is suggested that the laboratory measurement of realistic excretion rates of zooplankton is difficult owing to their large fluctuations, but this is not the case with respiration rate.

Calcium and Phosphorus Homeostasis in Man

Serum calcium and phosphorus levels, urinary excretion rates of calcium, phosphorus, and cyclic adenosine monophosphate (cAMP), and plasma parathyroid hormone (PTH) concentrations were determined in 11 normal subjects and in nine patients maintained on long-term prednisone therapy for chronic obstructive pulmonary disease. These same determinations were repeated in five of the prednisone-treated patients during the course of a seven-day calcium infusion. Prior to the infusion, the prednisone-treated patients demonstrated significantly elevated serum levels of PTH (P less than .005) and increased rates of urinary phosphate and cAMP excreation (P less than .005) when compared with normal subjects. After initiation of calcium infusion, the previous elevations in all of these determinations decreased to near normal levels. These data suggest that the effects of secondary hyperparathyroidism in patients maintained on long-term prednisone therapy may be overcome when calcium is administered intravenously.

Changes in the renal and extrarenal handling of phosphate induced by disodium etidronate (EHDP) in man.

1. The diphosphonate, disodium etidronate (disodium ethane-1-hydroxy-1, 1-diphosphonate; (EHDP), is known to increase plasma inorganic phosphate in man. The present study examines the mechanism of this effect. 2. When EHDP was given by mouth at a dose of 80 mumol (20 mg) kg-minus 1day-minus 1, plasma phosphate was significantly increased 24 h after the first dose but did not reach its maximum value for 2-3 weeks. When the drug was stopped, plasma phosphate returned to pretreatment values within 3 weeks. 3. Urinary excretion rate of phosphate was not greatly changed during treatment with EHDP despite the large increase in plasma phosphate, suggesting an alteration in renal handling. This was examined directly by infusing phosphate and inulin in six patients off and on EDPH. 4. EHDP had no effect on glomerular filtration rate (GFR) but produced a large increase in the maximum rate of renal tubular reabsorption of phosphate (TmP). The ratio Tm,P/GFR increased from a mean value of 1.15 mmol/1 to 2.10 mmol/1 on EHDP. This increase accounted for the hyperphosphataemia. 5. The same amount of phosphate infused at the same rate produced a greater rise in plasma phosphate when patients were on EHDP than when they were not, indicating a reduced net rate of entry of phosphate into tissues other than kidney. 6. Fasting total plasma calcium concentration and urine calcium excretion rate were not significantly altered by EHDP but the ability of infused phosphate to decrease plasma calcium was diminished. 7. It is suggested that EHDP alters phosphate transport in kidney and other tissues by a mechanism which is probably independent of the known hormonal influences on phosphate metabolism.