Advanced CKD with decreased urinary excretion of phosphate is the most common cause of hyperphosphatemia. Other causes are listed in Table 21–9.
Table 21–9.Causes of hyperphosphatemia. ||Download (.pdf) Table 21–9. Causes of hyperphosphatemia.
Massive load of phosphate into the extracellular fluid
Laxatives or enemas containing phosphate
Intravenous phosphate supplement
Rhabdomyolysis (especially if chronic kidney disease coexists)
Cell lysis by chemotherapy of malignancy, particularly lymphoproliferative diseases
Metabolic acidosis (lactic acidosis, ketoacidosis)
Respiratory acidosis (phosphate incorporation into cells is disturbed)
Decreased excretion into urine
Chronic kidney disease
Acute kidney injury
Plasma cell myeloma
Hemolysis in vitro
The clinical manifestations are those of the underlying disorder or associated condition.
In addition to elevated phosphate, blood chemistry abnormalities are those of the underlying disease.
Treatment is directed at the underlying cause. Exogenous sources of phosphate, including enteral or parenteral nutrition and medications, should be reduced or eliminated. Dietary phosphate absorption can be reduced by oral phosphate binders, such as calcium carbonate, calcium acetate, sevelamer carbonate, lanthanum carbonate, and aluminum hydroxide. Sevelamer, lanthanum, and aluminum may be used in patients with hypercalcemia, although aluminum use should be limited to a few days because of the risk of aluminum accumulation and neurotoxicity. In acute kidney injury and advanced CKD, dialysis will reduce serum phosphate.
Patients with acute severe hyperphosphatemia require hospitalization for emergent therapy, possibly including dialysis. Concomitant illnesses, such as acute kidney injury or cell lysis, may necessitate admission.
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