Hyperphosphatemia

Young/Growing Animals: Often show physiologically elevated levels due to enhanced intestinal uptake and decreased renal excretion intended to facilitate bone mineralization.

Renal and Urinary Issues:
- Chronic Renal Failure: The most common cause in many monogastric species, excluding horses.
- Obstruction: Often indicates urinary tract obstruction.
Cellular and Tissue Damage:
- Cell Lysis: Release of phosphorus after the destruction of red blood cells or muscle cells (rhabdomyolysis).
- Dehydration: Hemoconcentration can lead to increased concentrations, though this may be partially masked by concurrent anorexia and reduced dietary intake.

- 1. Hypoparathyroidism: Absence of parathyroid hormone leads to increased renal phosphorus reabsorption.
  2. Enemas: Severe acute cases have been reported following the use of hypertonic sodium-phosphate enemas in humans and small ruminants.

Diagnostic Indicator: Primarily serves as a marker for other serious disease processes like severe muscle damage.
Secondary Electrolyte Imbalances:
- Hypocalcemia: Excessive phosphorus precipitates with calcium to form insoluble complexes.
- Hypomagnesemia: Also occurs due to the formation of mineral complexes.
Symptomatic Presentation: Severe cases with concomitant hypocalcemia can cause muscle fasciculations and tetanic muscle contractions.
Tissue Damage: Sustained hyperphosphatemia can lead to extraskeletal tissue mineralization, which has a potentially fatal outcome.

The Hemolysis Error: Hemolysis during or after collection releases intracellular phosphorus from red blood cells, yielding erroneously high results.
Sample Integrity: Hemolytic blood samples should never be used to determine serum or plasma inorganic phosphate (Pi) concentrations.

Page updated

Google Sites

Report abuse