No specific signs.

Usually identified on routine clinical laboratory studies and as a result of the presence of hypocalcemia.

Can follow ingestion of large amounts of phosphate containing laxatives for bowel preparation imaging studies, from perforation of the rectum from phosphate enemas and from excess administration of intravenous phosphate.

Acute phosphate nephropathy can occur with oral sodium phosphate.

Severe hyperphosphatemia, hypocalcemia, metabolic acidosis, acute renal failure, and mortality in children and certain adult population following phosphate containing Fleet enemas.

Phosphate containing enemas creates fluid movement into the rectal sigmoid area induced by highly osmotic sodium phosphate.

Generally, phosphate containing enemas cause rapid fluid movement and has little absorption of the enema contents, but rarely retention of the enema fluid may result in systemic auction of large quantities of sodium and phosphate.

Endogenous sources from tumor or muscle can increase phosphate levels.

May be secondary to inability of the excretion of phosphate as in acute or chronic renal failure.

All natural foods contain phosphate which can be cleared by normal kidneys, but when glomerular filtration rate falls below 20-30 mg d/L this function is impaired.

Upper gastrointestinal bleeding can provide large phosphate loads leading to hyperphosphatemia.

Can be caused by potassium phosphate preparations utilized to improve hypokalemia.

Transfusion of RBC’s which can lead to hemolysis ad the release of phosphate stores.

May result from destruction of large amounts of tissue such as with tumor lysis syndrome, acute rhabdomyolysis, and severe hemolysis from an autoimmune cause or blood group mismatch, with release of a large phosphate load into the extracellular space.

When large amounts of phosphate enter the extracellular space and other nephrotoxic substances such as hemoglobin, myoglobin, and uric acid reduce the ability of the kidney to clear the phosphate load leading to renal failure, hypocalcemia, seizures and even death.

Usually occurs abruptly and is associated with immediate and severe hypocalcemia which can commonly lead the seizures.

The principal mechanism for maintaining phosphate homeostasis is renal clearance.

Because PTH prevents phosphate reabsorption in the proximal kidney hypoparathyroidism is associated with high normal to elevated phosphate levels.

Associated with acromegaly.

Associated with tumoral calcinosis when kidney clearance of phosphate is impaired and calcium-phosphate salts accumulate around large joints.

Children and adolescents have higher serum levels of phosphate than do adults.

Preventing increases in serum phosphate beneficial in chronic kidney disease, given reports of greater adverse renal and cardiovascular outcomes in association with hyperphosphatemia and even modest elevations in serum phosphate within the normal range.

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