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Hyperphosphatemia

By

James L. Lewis III

, MD, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham

Last full review/revision Apr 2020| Content last modified Apr 2020
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Hyperphosphatemia is a serum phosphate concentration > 4.5 mg/dL (> 1.46 mmol/L). Causes include chronic kidney disease, hypoparathyroidism, and metabolic or respiratory acidosis. Clinical features may be due to accompanying hypocalcemia and include tetany. Diagnosis is by serum phosphate measurement. Treatment includes restriction of phosphate intake and administration of phosphate-binding antacids, such as calcium carbonate.

Etiology of Hyperphosphatemia

The usual cause of hyperphosphatemia is

  • Decrease in renal excretion of phosphate

Hyperphosphatemia occasionally results from a transcellular shift of phosphate into the extracellular space that is so large that the renal excretory capacity is overwhelmed. This transcellular shift occurs most frequently in

Hyperphosphatemia can also occur with excessive oral phosphate administration and occasionally with overzealous use of enemas containing phosphate.

Pathophysiology of Hyperphosphatemia

Hyperphosphatemia plays a critical role in the development of secondary hyperparathyroidism and renal osteodystrophy in patients with advanced chronic kidney disease Chronic Kidney Disease Chronic kidney disease (CKD) is long-standing, progressive deterioration of renal function. Symptoms develop slowly and in advanced stages include anorexia, nausea, vomiting, stomatitis, dysgeusia... read more Chronic Kidney Disease as well as in patients on dialysis.

Hyperphosphatemia can lead to calcium precipitation into soft tissues, especially when the serum calcium × phosphate product is chronically > 55 mg2/dL2 (4.4 mmol2/L2) in patients with chronic kidney disease. Soft-tissue calcification in the skin is one cause of excessive pruritis in patients with end-stage renal disease who are on chronic dialysis. Vascular calcification also occurs in dialysis patients with a chronically elevated calcium × phosphate product; this vascular calcification is a major risk factor for cardiovascular morbidity including stroke Overview of Stroke Strokes are a heterogeneous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurologic deficit. Strokes can be Ischemic (80%), typically resulting... read more Overview of Stroke , myocardial infarction Acute Myocardial Infarction (MI) Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without dyspnea, nausea, and diaphoresis.... read more Acute Myocardial Infarction (MI) , and claudication.

Symptoms and Signs of Hyperphosphatemia

Most patients with hyperphosphatemia are asymptomatic, although symptoms of hypocalcemia Symptoms and Signs Hypocalcemia is a total serum calcium concentration 8.8 mg/dL ( 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration 4.7 mg/dL ( 1.17... read more , including tetany, can occur when concomitant hypocalcemia is present. Soft-tissue calcifications are common among patients with chronic kidney disease; they manifest as easily palpable, hard, subcutaneous nodules often with overlying scratches. Imaging studies frequently show vascular calcifications lining major arteries.

Diagnosis of Hyperphosphatemia

  • Phosphate concentration > 4.5 mg/dL (> 1.46 mmol/L)

Hyperphosphatemia is diagnosed by phosphate concentration. When the etiology is not obvious (eg, rhabdomyolysis, tumor lysis syndrome, renal failure, overingestion of phosphate-containing laxatives), additional evaluation is warranted to exclude hypoparathyroidism or pseudohypoparathyroidism Pseudohypoparathyroidism Hypocalcemia is a total serum calcium concentration 8.8 mg/dL ( 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration 4.7 mg/dL ( 1.17... read more , which is end-organ resistance to parathyroid hormone (PTH). False elevation of serum phosphate also should be excluded by measuring serum protein, lipid, and bilirubin concentrations.

Treatment of Hyperphosphatemia

  • Phosphate restriction

  • Phosphate binders

  • Sometimes saline diuresis or hemodialysis

The mainstay of treatment in patients with advanced chronic kidney disease is reduction of phosphate intake, which is usually accomplished with avoidance of foods containing high amounts of phosphate and with use of phosphate-binding drugs taken with meals. Although quite effective, aluminum-containing antacids should not be used as phosphate binding agents in patients with end-stage renal disease because of the possibility of aluminum-related dementia and osteomalacia.

Calcium carbonate and calcium acetate are frequently used as phosphate binders. But their use requires close monitoring because of the possibility of excessive calcium × phosphate product causing vascular calcification in dialysis patients taking calcium-containing binders.

A phosphate-binding resin without calcium, sevelamer, is widely used in dialysis patients in doses of 800 to 2400 mg orally 3 times a day with meals. Lanthanum carbonate is another phosphate binder that lacks calcium and is used in dialysis patients. It is given in doses of 500 to 1000 mg orally 3 times a day with meals.

Sucroferric oxyhydroxide combines the need many dialysis patients have for elemental iron with phosphate binding. It is given in doses of 500 mg orally 3 times a day with meals.

Hemodialysis Hemodialysis In hemodialysis, a patient’s blood is pumped into a dialyzer containing 2 fluid compartments configured as bundles of hollow fiber capillary tubes or as parallel, sandwiched sheets of semipermeable... read more does remove some phosphate, but not enough to allow most patients with end-stage renal disease to avoid significant hyperphosphatemia without dietary interventions.

Saline diuresis can be used to enhance phosphate elimination in cases of acute hyperphosphatemia in patients with intact kidney function. Hemodialysis can lower phosphate levels in cases of severe acute hyperphosphatemia.

Key Points

  • The usual cause of hyperphosphatemia is advanced renal insufficiency; hypoparathyroidism and pseudohypoparathyroidism are less common causes.

  • Most patients are asymptomatic, but those who also are hypocalcemic may have tetany.

  • Treat by restricting dietary phosphate and sometimes with phosphate binders.

  • Saline diuresis or hemodialysis may be needed.

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