1. VANESSA WICKHAM AND NEIL BARRY
HYPERPHOSPHATEMIA
VANESSA WICKHAM AND NEIL BARRY

2. WHAT IS PHOSPHOROUS
Phosphorus is the sixth most abundant element in the human body. A highly reactive substance, it occurs in nature, including in the human body, as phosphate.
Phosphorus (phosphate) is critical for bone mineralization, cellular structure, genetic coding, and energy metabolism.
The adult body contains approximately 1000 g of phosphorus, of which 80-90% is in bone. An additional 10-14% is intracellular and the remaining 1% is extracellular.

3. WHAT IS HYPERPHOSPHATEMIA
Hyper-excess
Phosphatemia-phosphate levels in blood serum
Thus, this can be defined as abnormally high levels of phosphate in the blood.
This is usually coupled with HYPO-calcemia, as the body attempts to maintain dynamic equilibrium between calcium and phosphate levels.
Hyperphosphatemia is considered significant when levels are greater than 5 mg/dL in adults or 7 mg/dL in children or adolescents.

4. ETIOLOGY
The most common cause of hyperphosphatemia is renal failure. Less common causes can be classified according to pathogenesis;
ie, increased phosphate intake,
decreased phosphate output,
or a shift of phosphate from the intracellular to the extracellular space.
Often, several mechanisms contribute. Impaired renal excretion is most frequently the major factor, with relatively increased intake or cell breakdown contributing to the problem

5. Increased intake This can result from the following:
Excessive oral or rectal use of an oral phosphate-saline laxative (Phospho-soda)
Excessive parenteral administration of phosphate
Milk-alkali syndrome
Vitamin D intoxication

6. Decreased excretion This can result from the following:
Renal failure, acute or chronic
Hypoparathyroidism
Pseudohypoparathyroidism
Severe hypomagnesemia
Tumoral calcinosis
Bisphosphonate therapy

7. Shift of phosphate from intracellular to extracellular space
This can result from the following:
Rhabdomyolysis- breakdown of skeletal muscle
Tumor lysis
Acute hemolysis – destruction of red blood cells
Acute metabolic or respiratory acidosis – increase of blood pH

8. PATHOPHYSIOLOGY
Hyperphosphatemia occurs when the phosphorus load (from GI absorption, exogenous administration, or cellular release) exceeds renal excretion and tissue uptake, an imbalance that can result from any of the following 3 pathogenic mechanisms:
Excessive phosphate intake
Decreased phosphate excretion
Phosphate shift from intracellular to extracellular space

9. Clinical Presentation
Typically, most patients with hyperphosphatemia are asymptomatic. Signs and symptoms of acute hyperphosphatemia result from the effects of hypocalcemia, with patients occasionally reporting symptoms such as muscle cramps, tetany, and perioral numbness or tingling. Other symptoms include bone and joint pain, pruritus, and rash.
patients report symptoms related to the underlying cause of the hyperphosphatemia, generally uremic symptoms such as fatigue, shortness of breath, anorexia, nausea, vomiting, and sleep disturbances.

10. Evaluatin History with regard to use of the following: Antacids
Bisphosphonates
Potassium phosphate
Oral phosphate binders

11. Diagnosis
The following measurements are indicated in patients with hyperphosphatemia:
Serum phosphate level: Reference range in adults, mg/dL; reference range in children, 3-6 mg/dL; hemolysis or hyperlipidemia of the serum sample may lead to falsely elevated phosphorus levels
Serum calcium level
Electrolytes
Blood urea nitrogen (BUN) and creatinine levels
Serum magnesium level (may be low)

12. Treatment
The major strategies for treating hyperphosphatemia are as follows:
Diagnosis of the cause in order to initiate specific therapy: Eg, patients with hyperphosphatemia due to administration of liposomal amphotericin B who continue to require antifungal therapy may be switched to the formulation amphotericin B lipid complex, which contains less inorganic phosphate.
Limitation of phosphate intake: Patients with chronic kidney disease are advised to avoid foods that are especially high in phosphate; high-phosphate foods include dairy products; meats, nuts, and other high-protein foods; processed foods; and dark colas
Enhancement of renal excretion of phosphate: Hyperphosphatemia due to tumor lysis responds to enhancement of urinary losses through forced saline diuresis

13. Surgical Care
Surgery may sometimes be required for removal of large calcium phosphate deposits occurring in patients with tumoral calcinosis or long-standing renal failure. Perform parathyroidectomy in patients with renal failure who have tertiary (autonomous) hyperparathyroidism complicated by hypercalcemia, hyperphosphatemia, and severe bone disease.

14. Medication
Oral phosphate binders - to decrease gastrointestinal absorption of phosphorus.
Calcium salts- are effective but may produce hypercalcemia.
Aluminum salts are effective binders but may induce aluminum toxicity.
Acetazolamide is particularly efficient in promoting renal phosphate excretion.

15. References
Block GA, Wheeler DC, Persky MS, et al. Effects of phosphate binders in moderate CKD. J Am Soc Nephrol Aug. 23(8): [Medline]. [Full Text].
Shutto Y, Shimada M, Kitajima M, Yamabe H, Saitoh Y, Saitoh H, et al. Inadequate Awareness among Chronic Kidney Disease Patients Regarding Food and Drinks Containing Artificially Added Phosphate. PLoS One Nov 13. 8(11):e [Medline]. [Full Text].
Marraffa JM, Hui A, Stork CM. Severe hyperphosphatemia and hypocalcemia following the rectal administration of a phosphate-containing Fleet pediatric enema. Pediatr Emerg Care Jul. 20(7): [Medline].
[Guideline] Hawley C. Serum phosphate. Nephrology. Apr (S1):S201-5.
Sutherland SM, Hong DK, Balagtas J, Gutierrez K, Dvorak CC, Sarwal M. Liposomal amphotericin B associated with severe hyperphosphatemia. Pediatr Infect Dis J Jan. 27(1):77-9. [Medline].