Hyperphosphatemia is abnormally high levels of phosphate in the blood, possibly due to increased phosphate intake, decreased phosphate excretion, or a disorder that shifts intracellular phosphate to the extracellular space.
However, severe hyperphosphatemia is, for the most part, clinically asymptomatic. Morbidity in patients with this condition is associated more frequently with an underlying disease than increased phosphate values.
Signs and symptoms
Although most patients with Hyperphosphatemia are asymptomatic, they sometimes report symptoms of hypocalcemia, such as muscle cramps, tetany, and perioral or tingling numbness. Other symptoms include bone and joint pain, pruritus, and rash.
More commonly, patients report symptoms related to the underlying cause of Hyperphosphatemia. These are usually uraemic symptoms, such as the following:
- Difficulty breathing.
- Sleep disorders
In acute hyperphosphatemia, especially that caused by the administration of parenteral phosphate, the patient may be hypotensive or show signs of hypocalcemia, such as the following:
- Positive Trousseau or Chvostek sign.
- Carpopedal spasm.
The results of a complete chemical profile can be used to determine the cause of Hyperphosphatemia:
Low levels of calcium and high phosphate levels were observed with renal failure and hypoparathyroidism. Blood urea nitrogen and creatinine: helps determine if renal failure is the cause of Hyperphosphatemia.
High levels of intact parathyroid hormone (HPI): higher probability in patients with renal failure. Relatively low levels of intact HPI and normal renal function: have been found in patients with primary or acquired hypoparathyroidism.
Serum Calcium and Phosphate elevated levels were observed with: vitamin D intoxication and milk and alkaline syndrome.
Relatively low levels of HPI and high 25 and vitamin D: 1.25 Are also observed in vitamin D intoxication.
Low HPI and vitamin D levels are seen in milk and alkaline syndrome.
There are other more unusual disorders, such as the following, which may also be considered as the cause:
- Vitamin D poisoning
- Laxative abuse (phosphonate).
- Tumor lysis
- Hypoparathyroidism isolated.
Rarely, if the cause of Hyperphosphatemia is not clear, a measurement of the urinary phosphate can be made within 24 hours. If the results indicate the following:
Fractional renal excretion more significant than 15%: suggests either massive ingestion of phosphate (e.g., laxative abuse [Fosfosoda] or lysis of tissues and the subsequent release of intracellular phosphate.
Fractional renal excretion not exceeding 15%: suggests that renal excretion deteriorates due to renal failure or hypoparathyroidism.
The main strategies for the treatment of Hyperphosphatemia are the following:
Diagnose and treat the cause: Hyperphosphatemia due to tumor lysis responds to forced saline diuresis to improve urinary losses.
Limit phosphate intake: renal failure is the clinical condition that most often requires the restriction of phosphate ingestion; Patients with advanced renal failure or complete renal failure also require phosphate binders to inhibit gastrointestinal absorption of phosphate.