Phosphorus, in serum

El 80 Toffaletti, J. (1984). Evaluation of the Kodak Ektachem analyzer method for phosphorus in serum. Clin. Chem. 30, 965, Abstr. 130. 

H25. Hunsberger, A., and Ferguson, L. K., Variations in phosphatase and inorganic phosphorus in serum during fracture repair. Arch. Surg. 24, 1052-1060 (1932). 

Plot the net absorbance of the standards against concentration using a spreadsheet (Chapters 3 and 16). From this plot and the net absorbance of the sample, determine the concentration of phosphorus in the protein-free filtrate. Multiply by 20 to obtain the concentration in the original serum sample. The normal range of phosphorus in serum is about 3.0 to 4.5 mg/dL for adults and 4.5 to 6.5 mg/dL for children. 

Pharmacologic therapy with sodium bicarbonate or citrate/citric acid preparations maybe needed in patients with stage 3 CKD or higher to replenish body stores of bicarbonate. Calcium carbonate and calcium acetate, used to bind phosphorus in sHPT, also aid in increasing serum bicarbonate levels, in conjunction with other agents. 

Because disturbances in fluid balance are routinely encountered in clinical medicine, it is essential to have a thorough understanding of body fluid compartments and the therapeutic use of fluids. Similarly, disturbances in serum sodium, potassium, calcium, phosphorus, and magnesium are ubiquitous and must be mastered by all clinicians. Dysregulation of fluid and/or electrolyte status has serious implications regarding the concepts of drug absorption, volumes of distribution, and toxicity. Similarly, many medications can disrupt fluid and/or electrolyte balance as an unintended consequence. 

Nephrotoxicity IDV potentially TDF Onset IDV—months after therapy TDF—weeks to months after therapy Symptoms IDV—asymptomatic rarely develop end-stage renal disease TDF—asymptomatic to symptoms of nephrogenic diabetes insipidus, Fanconi syndrome 1. History of renal disease 2. Concomitant use of nephrotoxic drugs Avoid use of other nephrotoxic drugs adequate hydration if on IDV monitor creatinine, urinalysis, serum potassium and phosphorus in patients at risk D/C offending agent, generally reversible supportive care electrolyte replacement as indicated... 

Risks associated with infusion of blood products include transfusion-related reactions, virus transmission (rare), hypocalcemia resulting from added citrate, elevations in serum potassium and phosphorus concentrations from use of stored blood that has hemolyzed, increased blood viscosity from supranormal hematocrit elevations, and hypothermia from failure to appropriately warm solutions before administration. 

One explanation for the adverse effects of excessive phosphorus intakes on bone health of rodents is that of secondary hyperthyroidism (4,j>,6). Under these circumstances, PTH activities and cAMP urinary excretions would be expected to increase and blood serum phosphorus would be expected to increase. This in turn would be expected to result in formation of calcium-phosphorus complexes, decrease in serum ionized calcium, parathyroid stimulation and bone resorption. 

Blood samples were centrifuged at 1000 x g for 20 min at 0-4°. Ionized calcium levels were immediately determined in serum and urine samples using a calcium ion-selective electrode (Ionetics, Inc., Costa Mesa, CA) urine volumes were recorded. The remaining serum and urine were aliquoted for various analyses and stored at -40°. Serum insulin was analysed by radioimmunoassay (Amersham Corp., Arlington Heights, IL). Serum levels of total calcium, phosphorus and creatinine as well as urine creatinine were determined by colorimetric procedures using an automated analyzer (Centrifichem, Baker Instruments Corp., Pleasantville, NY). Glomerular filtration rates (GFR) were calculated from serum and urine creatinine data GFR = urine creatinine/serum creatinine. 

Monitoring Closely monitor patients coinfected with HBV and HIV who discontinue tenofovir with both clinical and laboratory follow-up for at least several months. Monitor patients at risk for, or with a history of, renal dysfunction and patients receiving concomitant nephrotoxic agents for changes in serum creatinine and phosphorus. Consider bone monitoring for HIV infected patients who have a history of pathologic bone fracture or are at substantial risk for osteopenia. 

Renal osteodystrophy is a complex disorder with several pathogenic factors. Histological evidence of bone disease is common in early renal failure and deficits in calcitriol synthesis seems to be an important factor in the pathogenesis of secondary hyperparathyroidism in early CRF. The most common component is osteitis fibrosa manifested as subperiosteal resorption of bone. This is due to decreased excretion as well as increased secretion of parathyroid hormone. In CRF small increments of serum phosphorus cause small decreases in serum calcium. 

Mechanism of Action An antihyperphosphatemia agent that binds with dietary phosphorus in the GI tract, thus allowing phosphorus to be eliminated through the normal digestive process and decreasing the serum phosphorus level. Therapeutic Effect Decreases incidence of hypercalcemic episodes in patients receiving calcium acetate treatment. 

Sevelamer For control of serum phosphorus in patients with chronic kidney disease and hemodialysis... 

White Phosphorus. Decreased serum glucose levels were reported for some workers occupationally exposed to white phosphorus for a chronic duration (Ward 1928). Details of this study are provided in Section 2.2.2.2. 

White Phosphorus. No studies were located regarding absorption in humans or animals after inhalation exposure to white phosphorus. Human serum concentrations of phosphate (relevance to absorption of white phosphorus is unknown) following inhalation exposure are discussed in Section 2.3.3 (Metabolism). 

The serum phosphate level of a worker with phossy jaw was within the normal range of values for an adult human (Hughes et al. 1962). Excretion of phosphate via urinary and fecal routes was reported qualitatively to be approximately normal. The daily output of phosphorus in the feces was about 1/4 to 1/3 of the total output in both urine and feces. 

Phosphorus is found in every cell of the body, but most of it (about 80% of the total) is combined with calcium as Ca3(P04)2 in the bones and teeth (Harper 1969 Tietz 1970). Phosphorus is present in cells mainly as organic phosphate, with a small amount in serum as inorganic phosphate (Tietz 1970). Phosphorus is involved in the intermediary metabolism of carbohydrates (Tietz 1970). About 10% is found in combination with proteins, phospholipids, and carbohydrates and in other compounds in the blood and muscle (Harper 1969). The remaining phosphorus is widely distributed in various chemical compounds such as nucleic acids, nucleotides, and adenosine triphosphate (ATP) (Tietz 1970). 

The metabolism of phosphorus (P) is largely related to that of calcium (Ca). The Ca P ratio in the diet affects the absorption and excretion of these elements (Harper 1969). Any increase in serum phosphorus results in a decrease of serum calcium by mechanisms which are still unknown. For example, increased serum phosphorus levels and decreased serum calcium levels are seen in uremia (renal retention of phosphorus), hypoparathyroidism, hypocalcemia (decreased serum calcium levels), and hyperphosphatemia (increased serum phosphorus levels), and the reverse is seen in hypercalcemia (increased serum calcium levels) and hyperparathyroidism. Hypophosphatemia (low serum phosphorus levels) is seen in ricketts (vitamin D deficiency) (Harper 1969 Tietz 1970). 

J. Libeer, S. Scharpe, et al., Simultaneous determination of p-aminobenzoic acid and p-aminohippuric acid in serum and urine by capillary gas chromatography with use of a nitrogen-phosphorus detector, Clin. Chim. Acta, 775 119-123 (1981). 

H.C. De Bisschop and E. Michiels, Assay of the nerve agent soman in serum by capillary gas chromatography with nitrogen-phosphorus detection and splitless injection, Chromatographia, 18, 433-436 (1984). 

Vitamin D that is taken up by the fiver is converted to 25-hydroxyvitamin D by a microsomal hydroxylase (Fig. 30-3). 25-Hydroxyvitamin D is the main circulating form of vitamin D in the serum and the best indicator of vitamin D status. Normal serum levels are 14-60 ng/mL (35-150 nmol/L). When serum calcium concentrations decline, 25-hydroxyvitamin D is converted to 1,25-dihydroxyvitmin D by la-hydroxylase, a mixed-function oxidase that is located in the inner mitochondrial membrane in kidney tissue and whose expression is regulated by parathyroid hormone (PTH). The main function of 1,25-dihydroxyvitamin D is to increase the intestinal absorption of dietary calcium and phosphorus. When serum concentrations of calcium and phosphorus are normal or when large doses of vitamin D are administered, 25-hydroxyvitamin D is metabolized to 24,25-dihydroxyvitamin D in the renal... 

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