Common phosphate binders include aluminum hydroxide, calcium carbonate, and calcium acetate. In patients with chronic renal insufficiency, intestinal phosphate absorption should be reduced by administration of oral phosphate binders with a meal. Dietary phosphorus restriction should be initiated (usually with a protein-restricted diet ).
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All oral sources of phosphorus should be evaluated and adjusted. IV fluid therapy usually decreases circulating phosphorus levels by increasing the glomerular filtration rate, hence phosphorus excretion, preferred for vomiting and/or anorexic patients. Risk for soft tissue mineralization is higher when the calcium phosphorous (Ca × PO 4) product is greater than 70. Hyperphosphatemia may lead to hypocalcemia and soft tissue mineralization. Increases in phosphorous concentration usually lead to decreased calcium concentration. Hyperphosphatemia occurs when serum phosphorus concentrations are greater than 6.5 mg/dL, but reference ranges may vary like hypophosphatemia, the causes can vary (see Causes of Hyperphosphatemia). The underlying cause of hypophosphatemia should be investigated and addressed. Oral phosphorus supplementation may be provided, although it is generally ineffective in vomiting patients or those with diarrhea.
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Levels should be rechecked q6h to avoid oversupplementation, which may lead to hypocalcemia, soft tissue mineralization, hyperphosphatemia, or acute kidney injury. Monitor serum phosphorus concentration closely after discontinuing supplementation. Discontinue phosphorus supplementation when serum concentration normalizes. Phosphorus is best replaced by potassium phosphate CRI at 0.01 to 0.06 mmol/kg/hr IV mixed in saline or dextrose. When hypophosphatemia develops, phosphorus should be supplemented in symptomatic patients or asymptomatic patients at risk for symptomatic hypophosphatemia. In these patients, phosphorous levels should be monitored closely or supplemented. Hypophosphatemia should be anticipated in susceptible patients (ie, receiving insulin for diabetic ketoacidosis, at risk for refeeding syndrome). Hypophosphatemia may also cause impaired oxygen delivery, shortened platelet survival time, weakness, pain (associated with rhabdomyolysis), vomiting, and proximal tubule bicarbonate wasting. Hypophosphatemia decreases ATP concentrations in RBCs, increasing erythrocyte fragility and leading to hemolysis (generally not observed until phosphorus concentration is <1 mg/dL). Hypophosphatemia occurs when serum phosphorus concentrations are less than 2.5 mg/dL, although reference ranges vary (see Causes of Hypophosphatemia).