Hyperphosphatemia is the abnormal elevation of serum phosphate. The majority of the body's phosphate is stored in bone, while the remainder plays a critical role in the intracellular space as part of multiple proteins and, in the form of adenosine triphosphate (ATP), as part of energy stores. Serum phosphate levels are regulated by parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), vitamin D, and calcium. The most common cause of hyperphosphatemia is chronic kidney disease (CKD). In end-stage renal disease, CKD-mineral and bone disorder (CKD-MBD) leads to dysregulation of phosphate, calcium, and PTH, resulting in secondary hyperparathyroidism. Hyperphosphatemia is often asymptomatic and diagnosed serologically. Clinical features of severe hyperphosphatemia are often related to hypocalcemia. In addition, insoluble calcium phosphate formation can lead to nephrocalcinosis and calcinosis cutis. Treatment of hyperphosphatemia centers around treating the underlying cause and may also include IV fluids, hemodialysis, and, in selected cases, pharmacotherapy (e.g., phosphate binders).
The causes of hyperphosphatemia listed below have been grouped by mechanism.
- Often asymptomatic
- Symptoms are often related to concomitant: 
- Hypocalcemia: e.g., paresthesias, muscle spasms, cardiac arrhythmias
- Nephrolithiasis: e.g., renal colic, hematuria, dysuria
- Calcifications under the skin (i.e., calcinosis cutis) and in other tissues: e.g., localized pruritus and pain 
High phosphate levels cause the formation of insoluble calcium phosphate, which can lead to hypocalcemia, nephrolithiasis, and tissue calcifications.
- Hyperphosphatemia is often identified incidentally on laboratory studies.
- The diagnostic evaluation focuses on identifying the underlying cause.
- Evaluate for renal failure (most common cause).
- Obtain a detailed medical history (e.g., family medical history and medication use).
- Consider additional studies if renal function is normal or only mildly decreased.
If hyperphosphatemia is out of proportion to renal dysfunction, additional diagnostics should be obtained to identify the underlying cause. 
Routine studies 
Additional studies 
- Measure PTH.
- Elevated PTH : consistent with ↑ intestinal absorption, transcellular shifts, pseudohypoparathyroidism
- Normal or low PTH: Measure serum/urine calcium.
- Low calcium: suggestive of hypoparathyroidism
- Normal calcium: suggestive of pseudohyperphosphatemia or HFTC
- Elevated calcium: suggestive of non-PTH mediated hypercalcemia
- If the cause is still unclear, consider the following:
- Magnesium levels
- Diagnostics for rhabdomyolysis: e.g., creatine phosphokinase
- Hemolysis workup: e.g., CBC, reticulocytes
- Diagnostics for pseudohyperparathyroidism: e.g., liver chemistries and lipid panel
- Diagnostics for non-PTH mediated hypercalcemia: e.g., ionized calcium, vitamin D levels
General principles 
Consult nephrology to guide management.
- All patients
- Patients with chronic hyperphosphatemia: (e.g., resulting from CKD-MBD): Consider pharmacotherapy, including phosphate binders (e.g., sevelamer, calcium acetate).
- Patients with severe hyperphosphatemia (i.e., serum phosphate > 6.25 mg/dL)
Pharmacotherapy is usually reserved for patients with chronic hyperphosphatemia (e.g., patients with CKD-MBD) if dietary changes and/or hemodialysis do not maintain normal phosphate levels.
Oral phosphate binders
- Calcium acetate 
- Aluminum hydroxide (not commonly used because of the potential for aluminum toxicity)
- Adverse effects include: nausea, vomiting, diarrhea, constipation, abdominal pain, and hypophosphatemia
Additional agents are used in the management of hyperparathyroidism.
- Vitamin D: e.g., calcitriol, paricalcitol, doxercalciferol
- Calcimimetics: e.g., cinacalcet, etelcalcetide