Hyperphosphatemia in adults is defined as a serum inorganic phosphate concentration exceeding 1.6 mmol/L.
Etiology
The common causes include:
- Acute or Chronic Renal Failure: Impaired renal excretion of phosphate.
- Hypoparathyroidism: Reduced urinary phosphate excretion.
- Vitamin D Toxicity: Vitamin D can enhance phosphate reabsorption in the intestines and kidneys.
- Hyperthyroidism: Can promote bone resorption.
- Conditions Causing Phosphate Shift to Extracellular Space: Such conditions include acute acidosis, skeletal muscle damage, hyperthermia, and malignant tumors.
Clinical Manifestations
Hyperphosphatemia itself does not produce specific clinical symptoms. Acute hyperphosphatemia increases the risk of calcium-phosphate precipitation, which can lead to soft tissue and renal calcification, potentially causing kidney failure. Hyperphosphatemia is often accompanied by hypocalcemia, and patients may experience clinical symptoms resulting from hypocalcemia, such as seizures, arrhythmias, and hypotension.
Treatment
In addition to addressing the underlying cause, asymptomatic hyperphosphatemia or hyperphosphatemia in patients with normal renal function does not require special treatment, as excess phosphate can be excreted through the kidneys. For acute renal failure or cases involving significant hyperphosphatemia, hemodialysis can be used to remove excess phosphate.
The treatment of chronic hyperphosphatemia includes dietary phosphate restriction and the administration of oral phosphate binders, such as calcium salts or aluminum hydroxide.