P 2.3 - 4.0 HIGH
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HYPERPHOSPHATEMIA, a serum phosphorus greater than 4. 5 mg/dL, although children and postmenopausal women may have minimally elevated levels that are not pathologic. Serum phosphorus should be measured from a fasting blood sample because carbohydrate loads decrease the serum value whereas increased oral phosphorus loads usually increase the serum value. Phosphorus is predominantly located in bone (approximately 85%); 14% is intracellular and 1% is in the ECF. Therefore, serum phosphorus levels are a poor indicator of the total body phosphorus.
Hyperphosphatemia is most commonly the result of renal failure. As the GFR decreases to less than 30 ml/min, renal phosphorus excretion decreases dramatically. Other causes include hypoparathyroidism, pseudohypoparathyroidism, hyperthyroidism, rhabdomyolysis, acidosis, acromegaly, and tumor lysis syndrome. Spurious elevations are seen with analysis of samples that have been subjected to prolonged refrigeration or delays in processing; hemolyzed samples; or samples contaminated with hyperbilirubinemia, hyperlipidemia, dysproteinemias, heparin, or detergents.
Symptoms are most often secondary to hyperphosphatemia-induced hypocalcemia and include tetany and seizures. Precipitation with calcium causes soft tissue calcifications and is seen in patients with chronic renal failure, hypoparathyroidism, and tumor calcinosis (a rare syndrome seen in young black males that is characterized by normal serum calcium and PTH levels with ectopic calcifications around the large joints). Soft tissue calcifications occur when the calcium-phosphate product (serum calcium mg/dL x serum phosphate mg/dL) exceeds 70mg/dL. Such calcifications commonly occur in the heart, blood vessels, lungs, cornea, kidneys, and gastric mucosa. In patients with chronic renal failure, hyperphosphatemia is linked to increased morbidity and mortality.
Prevention of hyperphosphatemia entails restriction of dietary phosphate to 0. 6-0. 9 g/day and oral phosphate binders. Oral phosphate binders include calcium carbonate, calcium acetate, sevelamer, and lanthanum carbonate. Emergency treatment of acute severe hyperphosphatemia with associated symptomatic hypocalcemia includes the use of isotonic saline to induce increased urinary phosphate excretion provided renal failure is not present. In patients with renal failure who are awaiting dialysis, emergent temporary correction of hyperphosphatemia may be accomplished with infusion of glucose and insulin to promote cellular uptake; however, definitive treatment is with dialysis.