Phosphates excretion

Male rats given single, oral doses of 14 mg/kg [l-14C]tributyl phosphate excreted 50% of the label in urine, 10% in exhaled air as C02, and 6% in the feces within 1 day (Suzuki et al. 1984a). Within 5 days, cumulative radioactivity in urine, exhaled C02, and feces accounted for approximately 68%, 10%, and 10% of the administered radioactivity, respectively. 

Parathyroid hormone stimulates bone resorption by increasing the number and activity of osteoclasts. This demineralization process in the bone releases calcium and phosphate into the blood. Although the action of PTH on the bone appears to increase blood phosphate, its action on the kidney, which increases phosphate excretion in the urine, more than compensates for this increase and the net effect is a decrease in serum phosphate. 

In 1978, on the basis of a few measurements of urine calcium and phosphate excretion as well as an awareness of the previously mentioned work regarding the amounts of calcium and phosphate normally accreted in utero and postnatally, it became apparent that the demineralization, fractures and rickets we were seeing in our infants were caused by calcium deficiency. Consequently we increased the amount of calcium added to the parenteral alimentation solutions. If more than 12.5 mM of the calcium were added to a liter of hyperalimentation solution, gross precipitation would occur in the feeding solution. If 10 mM of calcium were added per liter, crystalline precipitated began to build up on the inside of our barium-impregnated silicone rubber central venous catheters. This crystalline precipitate resulted in gradual occlusion and functional loss of these lines. After several false starts and six lost catheters, chemical and crystal analysis showed that the precipitate inside these catheters was CaHPO. ... 

In the absence of renal tubular defects, measuring the concentrations of calcium and phosphate excreted in any individual infant s urine indicated in which direction the Ca/P ratio should be changed to achieve this fine-tuning. When the Ca/P ratio is appropriate, both calcium and phosphate should be measurable absence of measurable calcium or phosphate in the urine means the ratio must be changed. 

The polypeptide parathormone is released from the parathyroid glands when plasma Ca + level falls. It stimulates osteoclasts to increase bone resorption in the kidneys, it promotes calcium reabsorption, while phosphate excretion is enhanced. As blood phosphate concentration diminishes, the tendency of calcium to precipitate as bone mineral decreases. By stimulating the formation of vit D hormone, parathormone has an indirect effect on the enteral uptake of Ca + and phosphate. In parathormone deficiency, vitamin D can be used as a substitute that unlike parathormone, is effective orally. 

Furosemide (Lasix), torsemide (Demadex), and bumetanide (Bumex) possess some carbonic anhydrase inhibiting activity (about one-tenth that of chlorothiazide). This property may account for the increased bicarbonate and phosphate excretion seen after large doses of these diuretics. The elevated HCOj" loss probably indicates some proximal tubular effects for furosemide and bumetanide. 

Hypercalcemia, in contrast, results in calcitonin synthesis and release, while PTH release and formation of 1,25-(0H)2D2 are inhibited. Calcitonin inhibits bone resorption directly by reducing osteocyte activity. Calcitonin also induces an initial phosphate diuresis, followed by increased renal calcium, sodium, and phosphate excretion. 

Mechanism of Action A synthetic polypeptide hormone that acts on bone to mobilize calcium also acts on kidney to reduce calcium clearance, increase phosphate excretion. Therapeutic Effect Promotes an increased rate of release of calcium from bone into blood, stimulates new bone formation. 

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. 

PTH and l,25(OH)2D enhance renal retention of calcium, but PTH promotes renal phosphate excretion. FGF23 is a recently discovered hormone that stimulates renal phosphate excretion and inhibits renal production of l,25(OH)2D. Other... 

Kidney Decreased calcium excretion, increased phosphate excretion Calcium and phosphate excretion may be decreased by 25(OH)D and l,25(OH)2D1 Increased phosphate excretion... 

Parathormone) reabsoiption. phosphate excretion, and maintenance of serum calcium... 

The kidney regulates the acid-base balance of the body by control over resorption of sodium ions, which may exchange for hydrogen ions in the kidney tubule. Since most dietaries are of acid-ash, the urine is usually more acid than the original plasma filtrate and much of the phosphate excreted is thus changed to the acid monosodium salt, Within the range of normal variability, with an alkaline ash diet, the urine may become alkaline, and in extreme instances, some sodium bicarbonate may be excreted. 

Vitamin D. Vitamin D is a steroidlike hormone that can be obtained from dietary sources or synthesized in the skin from cholesterol derivatives in the presence of ultraviolet light. Vitamin D produces several metabolites that are important in bone mineral homeostasis.27,31 In general, vitamin D derivatives such as 1,25 dihydroxyvitamin D3 increase serum calcium and phosphate levels by increasing intestinal calcium and phosphate absorption and by decreasing renal calcium and phosphate excretion.27,46... 

PGE2 may also be involved in renal phosphate excretion, because exogenous PGE2 antagonizes the inhibition of phosphate resorption by parathyroid hormone in the proximal tubule. However, the physiologic role of this eicosanoid may be limited because the proximal tubule, the major site for phosphate transport, produces few prostaglandins. 

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). 

No studies on body burden reduction methods were located. The state of definitive knowledge of white phosphorus metabolism is too limited to permit extensive speculation on methods for reducing body burden. However, it is possible that increasing selective excretion of phosphate may increase the rate of inorganic conversion of white phosphorus to phosphate (this conversion is described in detail in Section 2.3). Since phosphate is a naturally occurring component of the blood s buffering system, this would effectively deactivate the phosphorus. No methods for selectively increasing phosphate excretion were located. 

Because the kidney is the only significant source of la-OHase, inadequate formation of l,25-(OH)2D3 occurs in renal failure [168], Not only is the mass of kidney tissue and therefore of enzyme decreased, but also with renal failure, phosphate excretion is reduced and serum phosphate rises. Increased phosphate inhibits la-OHase so that little l,25-(OH)2D3 is formed. Acidosis, a frequent result of renal failure, also impairs la-OHase activity [169, 170]. Deficiency of the active form of vitamin D causes osteomalacia, a prominent feature of renal osteodystrophy. Therapy is directed toward use of l,25-(OH)2D3, reduction of serum phosphate, and correction of acidosis, so that residual la-OHase can be expressed. 

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... 

Disposition in the Body. Absorbed from the gastro-intestinal tract and converted to the active form, pyridoxal phosphate. Excreted in the urine mainly as 4-pyridoxic acid. 

Ikeda, T., and Mitchell, A. W. (1982). Oxygen uptake, ammonia excretion and phosphate excretion by kriU and other Antarctic zooplankton in relation to their body size and chemical composition. 

Ikeda, T., Hing Fay, E., Hutchinson, S. A., and Boto, G. M. (1982). Ammonia and inorganic phosphate excretion by zooplankton from inshore waters of the Great Barrier Reef I. Relationship... 

FUNCTION Maintains the level of calcium in the blood, acting mainly on bone and kidney. In bone, PTH stimulates osteoclast cells to produce bone breakdown with release of calcium and phosphorus (PTH has a similar effect in this regard as vitamin D, but operates by a different mechanism PTH acts through cyclic AMP). In the kidney, PTH increases calcium reabsorption and phosphate excretion (vitamin D, however, increases absorption of both calcium and phosphorus in the kidney). 

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. ... 

Decreased renal phosphate excretion Decreased glomerular filtration rate Renal failure, chronic and acute Increased tubular reabsorption Hypoparathyroidism Pseudohypoparathyroidism Acromegaly Disodium etidronate Increased phosphate intalce... 

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. 

In contrast to the calcium-conserving effect of PTH on the kidneys, PTH increases renal phosphate excretion at the proximal tubule by directly lowering the renal phosphate threshold. Approximately 6.5 g (210 mmol) of phosphate is filtered by the kidneys each day. Normally, 85% to 90% is reabsorbed by the renal tubules (proximal and distal convoluted tubule). PTH is one of the most important factors regulating the renal phosphate threshold and hence the serum phosphate concentration. 

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