Physiologically elevated serum and plasma Pi concentrations are observed in young and growing animals due to enhanced intestinal phosphorus uptake and decreased renal phosphorus excretion, presumably to facilitate bone mineralization. Pathologically increased extracellular phosphorus concentrations can be the result of hemoconcentration, decreased renal excretion, decreased intracellular uptake, or cellular release of phosphorus following cell lysis. Decreased urinary phosphorus excretion in association with chronic renal failure is the most common cause of hyperphosphatemia in many monogastric species except horses. In ruminants, hyperphosphatemia is commonly seen in dehydrated animals and is most likely due to hemoconcentration and a concomitant reduction in saliva production. Massive tissue injury with rhabdomyolysis results in damaged cell membrane integrity, which leads to release of phosphorus together with other predominantly intracellular compounds such as potassium into the extracellular space. Hypoparathyroidism may result in hyperphosphatemia due to increased renal phosphorus reabsorption in the absence of PTH. Incidental cases of severe acute hyperphosphatemia were reported after repeated treatment with enemas containing hypertonic sodium phosphate solutions in people and small ruminants.
Hemolysis occurring during or after blood sample collection results in release of intracellular phosphorus from RBC and therefore gives erroneously high serum Pi concentrations. Therefore, hemolytic blood samples should not be used to determine the serum or plasma Pi concentration.
Hyperphosphatemia as it occurs during hemoconcentration or decreased glomerular filtration is unlikely to be of any clinical relevance. In more severe cases, concomitant hypocalcemia may result from precipitation of excessive phosphorus with calcium and cause muscle fasciculations and tetanic muscle contractions. In sustained cases, precipitation of calcium-phosphate salts results in extraskeletal tissue mineralization with a potentially fatal outcome.
Last full review/revision July 2011 by Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM