Phosphates urinary

A recent method to screen the urine for alkyl phosphates as an indicator of exposure to organophosphate insecticides shows that the method can be used to determine environmental exposure to a specific organophosphate pesticide. The method was found to be sensitive, identifying low levels of exposure to insecticides in the environment by quantitation of urinary phosphates (Davies and Peterson 1997). The test is limited in that it is only useful for assessing recent exposure, due to the short half-life of the organophosphate pesticides. 

Inhibitors should be removed from sample. An example is urinary phosphate, which can be removed by dialysis prior to measuring the urinary alkaline phosphatase activity (18). 

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. 

No studies were located that specifically address white phosphorus metabolism in humans or animals following dermal white phosphorus bums. However, orthophosphate is a stable end-product of the oxidation and hydrolysis of white phosphorus. Thus, it is appropriate to examine data on serum phosphate and urinary phosphate in humans and animals following dermal white phosphorus burns (these data are discussed further in Section 2.2). 

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). 

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). 

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. ... 

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). 

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. 

Howard et al. (Hll, H12), who suggested that the rise in plasma phosphate produced by intravenous calcium was due to parathyroid suppression, and that this rise was smaller than normal in hyperparathyroidism. It has since been shown that the effect of intravenous calcium on plasma phosphate is not a measure of parathyroid activity (N5), and this may explain why calcium infusions have tended to fall into disfavor. The fall in urine phosphate which follows calcium infusion does, however, indicate parathyroid suppression (K5, N5). Table 5 shows the effect of a standard calcium infusion on the urinary phosphate/creatinine ratio... 

Fic. 14. Effect of calcium infusion upon urinary phosphate/creatinine ratio in six cases of primary hyperparathjroidism compared with same effect in 14 normal subjects. 

The natriuretic effect of prestegane B observed in vivo [306] could have to do with the inhibition of Na+/K+-ATP activity demonstrated in vitro in previous studies. This synthetic lignan probably acts beyond the proximal tubule, as urinary phosphate was not altered. Prestegane B mimics the effects of other endogenous diuretic and natriuretic hormones, but its site of action and its effect on renal hemodynamics are obviously different. 

Brown, D.R., Donavan, E.F., Tsang, R.C., Bobik, C.M., Chen, I.-W., and Johnson, J.R., 1978 Urinary phosphate and cyclic AMP excretion following citrate-induced hypocalcemic stimulation of the neonatal parathyroid glands, J.Pediatr. 93 842 Kreuger, A., 1976 Adenine metabolism during and after exchange transfusions in newborn infants with CPD-Adenine blood. Transfusion 16 249... 

The urinary phosphates are derived from ingested inorganic phosphate as well as from the breakdown of phosphoprotein and cellular material such as phospholipid and sugar phosphates. In an alkaline urine in which base is being excreted by the kidney, phosphate excretion may be... 

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. 

Estimation of Phosphate.— Urinary phosphate may be rapidly and roughly estimated by means of uranium acetate. Measure 1 ml. of an accurately prepared 3-50 per cent, uranium acetate solution into a test tube. Dilute with 3-4 ml. water. Add 2-3 drops of 5 per cent, potassium ferrocyanide. A brown precipitate... 

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