Urinary phosphate excretion

Carbonic anhydrase inhibitors have been used as adjuvants in the treatment of epilepsy and in some forms of hypokalemic periodic paralysis and to increase urinary phosphate excretion during severe hyperphosphatemia. 

Urinary phosphate was measured in eight human cases of dermal white phosphoms bum following explosion of incendiary munitions. It was not possible to estimate doses. The rate of urinary phosphate excretion varied widely, ranging between 0.08 and 5.83 g/day. The normal adult human output of inorganic phosphate in urine is 0.34—1.0 g/day (Henry 1967). 

Normally less than 20% of the filtered load of phosphate is excreted into the urine, but above a plasma phosphate concentration of approximately 1.2mmol/L increments in urinary phosphate excretion increase linearly with the filtered load, suggesting that there is Tn, (tubular maximal uptake) for phosphate. Predictably the T , for phosphate is influenced by the circulating PTH concentration and the ratio of T for phosphate to GFR (T ,P/GFR). T,nP/GFR has been used as a test in the differential diagnosis of hypercalcemia. Although superseded in this context by modern PTH assays, it may still be useful in the investigation of inherited disorders of tubular phosphate handling. ... 

Urine should be collected in 6 mol/L HCl, 20 to 30 ml for a 24-hour specimen, to avoid precipitation of phosphate complexes. Simultaneous measurement of phosphate and creatinine in serum and urine with fasting morning spot or 1- to 2-hour timed collections permits calculation of the renal phosphate threshold (TmPO /GFR). The clearance of phosphate divided by creatinine clearance can be plotted on a nomogram, and the TmP04/GFR determined. This index expresses phosphate reabsorption as a function of both serum phosphate concentration and GFR and is more useful than urinary phosphate excretion. 

Kemp GJ, Blumsohn A, Morris BW. Circadian changes in plasma phosphate concentration, urinary phosphate excretion and cellular phosphate shifts. 

This hormone is secreted by the parathyroid glands, which are four in number and lie on the posterior surface of the thyroid gland. The exact manner in which the hormone exerts its action upon calcium and phosphorus metabolism has not been proved satisfactorily, but the most immediate effect of administration of parathyroid extract which has been generally observed is an increased excretion of phosphorus in the urine, which is accompanied by a lowering of the serum inorganic phosphate. The increase in the urinary phosphate excretion has been ascribed by Harrison and Har-... 

The effect of parathyroid hormone upon bone is considered by Albright to be secondary to the increase in urinary phosphate excretion, the depletion of serum phosphate causing accelerated resorption of phosphate from bone which is inevitably accompanied by increased calcium resorption. This author distinguishes between hyperparathyroidism with bone disease and a like condition without bone disease. In the former there is an increase in the resorption of bone with a compensatory increase in bone formation, the osteoblasts and osteoclasts being numerically increased and the phosphatase activity of the serum raised. The latter condition shows normal bone metabolism, and the increased calcium excretion is postulated to come entirely from increased calcium intake and absorption, whereas serum phosphatase activity is normal. 

Since the source of protein appeared to affect the maximum kidney Ca level reached (Table XII) we decided to determine the effect of feeding, for 6 weeks, soy assay protein or spray-dried egg white on kidney calcification in rats. The results are summarized in Table XIV. To our surprise kidneys of male and female rats fed egg white powder showed a normal Ca content. It is likely that the increased urinary sulphate excretion by rats fed egg white (28) prevented the precipitation of calcium phosphate in the... 

Tumor-induced osteomalacia (oncogenic hypophosphatemic osteomalacia) is also characterized by excessive urinary excretion of phosphate, and hence hypophosphatemia and low circulating calcitriol. Removal of the tumor results in normalization of phosphate excretion and... 

CAIs alter renal function primarily by inhibiting carbonic anhydrase in the proximal tubule, which results in decreased bicarbonate reabsorption. The net effect of the renal actions of acetazolamide therapy is alkaliniza-tion of the urine and metabolic acidosis. Metabolic acidosis results from the initial bicarbonate loss and persists with continued acetazolamide use. Moderate metabolic acidosis develops in most patients. Reabsorption of bicarbonate independent of carbonic anhydrase prevents severe acidosis. Initially, acetazolamide produces diuresis, but urinary output decreases with the development of metabolic acidosis. In addition, decreased urinary citrate excretion follows acetazolamide therapy and has been attributed to the metabolic acidosis it produces. A high urinary pH and low urinary citrate concentration are conducive to precipitation of calcium phosphate in both the renal papillae and the urinary tract. 

Sodium cellulose phosphate (Calcisorb) binds calcium in the gut, reduces urinary calcium excretion and may benefit calcium stone-formers. 

Studies with baby pigs revealed that urinary Ca levels vt crc low and equivalent to about 2% of the intake, Fecal Ca was equivalent to about 21% of the intake. The remaining calcium was retained and used for growth. The excreted phosphate was more equally distributed in the urine and feces, w here the urinary phosphate was equivalent to 12 to i7% of the intake and the fecal phosphate to about 13% of the intake. The remaining phosphate was used for growth (Miller ef al, 1964). 

Features of lithium-induced hyperparathyroidism include a) a low urinary calcium excretion and the absence of nephrolithiasis b) normal urinary cyclic adenosine monophosphate excretion and c) normal plasma inorganic phosphate [32]. In lithium-induced hypercalcemia, a higher frequency of conduction defects has been noted [47]. Lithium also inhibits par-... 

Prolonged bed rest is associated with increased urinary nitrogen excretion. Calcium, sodium, potassium, phosphate, and sulfate excretions are increased hydrogen ion excretion is reduced, presumably caused by decreased metabolism of skeletal muscle. The amplitude of circadian variation of plasma cortisol is reduced by prolonged immobilization, and the urinary excretion of catecholamines may be reduced to one third of the concentration in an active individual. Vanil-lylmandehc acid excretion is reduced by one fourth after 2 to 3 weeks of bed rest. 

Urinary phosphate varies with age, muscle mass, renal function, PTH, the time of day, and other factors. Urinary excretion of phosphate varies widely with diet and is essentially equivalent to dietary intake. On a nonrestricted diet, the reference interval for urinary phosphate is 0.4 to 1.3 g/day (12.9 to 42.0 mmol/day). 

Carriers of OCT deficiency (estimated to be several thousand women in the U.S. A.) can be identified by administration of a single oral dose of allopurinol, a purine analogue, followed by measurement of urinary orotidine excretion. The underlying principle of this assay is that when the intramitochondrial carbamoyl phosphate accumulates in OCT heterozygotes, it diffuses into the cytoplasm stimulating the biosynthesis of pyrimidines. One of the intermediates in this pathway—orotidine—accumulates, leading to orotidinuria (Figure 17-8). 

As intestinal absorption of calcium increases, urinary calcium excretion also increases. When the latter exceeds 300 mg/d, formation of calcium phosphate or calcium oxalate stones (urolithiasis) may occur. Hypercalciuria may result from decreased reabsorption of calcium due to a renal tubular defect or from increased intestinal absorption of calcium. Hypercalciuria may be due to an intrinsic defect in the intestinal mucosa or secondary to increased synthesis of 1,25-(OH)2D in the kidney. Disordered regulation of 1,25-(0H)2D synthesis is relatively common in idiopathic hypercalciuria. Treatment usually includes reduction in dietary calcium. Increased vitamin D intake, hyperparathyroidism, and other disorders can also cause hypercalciuria and urolithiasis. 

C signal transduction pathway. Secretion of calcitonin is stimulated by hypercalcemia but the effect of the hormone on calcium transport appears to be secondary to increased phosphate uptake by target cells. The number and activity of osteoclasts are decreased, and urinary excretion of hy-droxyproline is decreased, Calcitonin may also inhibit release of calcium from the extracellular fluid calcium pool, but it increases calcium and phosphate excretion by renal tubules. Some tubular cells respond to calcitonin, PTH, and vasopressin, while others respond only to one or two of these hormones. In general, the actions of calcitonin in kidney and in bone are antagonistic to those of PTH. Calcitonin decreases secretion of gastrin and of gastric acid, and inhibits bile flow. 

Serum phosphorus concentration is so closely regulated by the kidneys that it is unusual for hyperphosphatemia (serum phosphorus concentration >4.5 mg/dL) to develop in patients with normal renal function. The most frequent causes of hyperphosphatemia are decreases in urinary phosphorus excretion, and increases in phosphate entrance into the extracellular fluid via either exogenous administration or endogenous intracellular phosphate release. 

EFFECTS ON URINARY EXCRETION Inhibitors of the Na -Cl symporter increase Na and CF excretion, but are only moderately efficacious (i.e., maximum excretion of filtered load of Na+ is only 5%) because -90% of the filtered Na load is reabsorbed before reaching the DCT. Some thiazide diuretics also are weak inhibitors of carbonic anhydrase, an effect that increases HCO and phosphate excretion and probably accounts for their weak proximal tubular effects. Inhibitors of the Na+-Cl symporter increase the excretion of and titratable acid by the same mechanisms discussed for loop diuretics. Acute administration of thiazides increases the excretion of uric acid, but uric acid excretion is reduced following chronic administration by the same mechanisms as for loop diuretics. Acute effects of inhibitors of the Na+-Cl symporter on Ca + excretion are variable when administered chronically, thiazide diuretics decrease Ca + excretion. The mechanism involves increased proximal reabsorption owing to volume depletion, as well as direct effects of thiazides to increase Ca + reabsorption in the DCT. Thiazide diuretics may cause a nfild mag-nesuria by a poorly understood mechanism. Since inhibitors of Na+-Q symport inhibit transport in the cortical diluting segment, thiazide diuretics attenuate the abdity of the kidney to excrete a... 

Berry GT, Palmieri M, Gross KC, Acosta PB, Hestenburg JA, Mazur A, Reynolds R, Segal S. The effect of dietary fruits and vegetables on urinary galactitol excretion in galactose-1-phosphate uridyltransferase deficiency. J Inherit Metab Dis 1993 16 91-100. 

Dang et al. (2000) increased the sensitivity of NAA for Th by separating the indicator radionuclide, Pa, using co-predpitations with manganese dioxide and barium sulfate and determined Th in total diet samples. A similar postirradiation procedure was coupled to the following pre-irradiation separation and concentration of Th (PC-RNAA) by H5llriegl et al. (2005) to increase the sensitivity of the method for the determination of urinary Th excretions. The pre-concentration procedure consisted of phosphate and caldum oxalate coprecipitations. The detection limit of Th in the urine sample was about 10 pg (0.04 jiBq). 

Although the major effect of parathormone is to mobilize calcium from bone, effects on other organs have also been described. Whereas the effect of parathormone on calcium mobilization is independent of any action of the hormone on the kidney, the phospha-turic action of parathormone is likely to result from a direct effect of the hormone on tubular excretion of phosphate. Parathyroidectomy leads to a decrease in urinary excretion of phosphate, and parathormone administration increases phosphate excretion in rats. An effect on glomerular filtration of phosphate was excluded, but it was established that parathormone acts on the tubular excretion of phosphate. 

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