Hyperphosphatemia in Animals

Hyperphosphatemia is defined as a blood phosphorus concentration that is above the reference range for the animal species in question. Although markedly elevated blood phosphorus concentrations for prolonged periods can also lead to secondary complications, such as soft tissue mineralization, hypocalcemia, and hypomagnesemia, because of formation of insoluble mineral complexes, hyperphosphatemia is primarily of concern as an indicator of other disease processes, such as urinary tract obstruction, severe muscle tissue damage, or hypoparathyroidism.

Physiologically elevated serum and plasma phosphorus concentrations are present in young and growing animals because of 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

• cellular release of phosphorus after cell lysis (eg: lysis of red blood or muscle cells)

Decreased urinary phosphorus excretion in association with chronic renal failure is the most common cause of hyperphosphatemia in many monogastric species, with the exception of horses. In ruminants, frank hyperphosphatemia is rare. However, it can occur in growing animals that are dehydrated.

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. However, because animals with dehydration or severe tissue damage are frequently also anorectic, hyperphosphatemia is at least partially masked by the decreased dietary phosphorus intake.

Hypoparathyroidism can result in hyperphosphatemia because of increased renal phosphorus reabsorption in the absence of parathyroid hormone. Incidental cases of severe acute hyperphosphatemia were reported after repeated treatment with enemas containing hypertonic sodium-phosphate solutions in humans and small ruminants (1).

Hemolysis occurring during or after blood sample collection results in release of intracellular phosphorus from RBCs and thereby gives erroneously high serum inorganic phosphate 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 can result from precipitation of excessive phosphorus with calcium, which can 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.