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Basics ⬇

Outline

BASICS

Overview!!navigator!!

Serum P concentration greater than the reference interval.

Pathophysiology

  • Kidneys, intestine, and skeleton are involved in P homeostasis in conjunction with diet and hormonal factors including PTH, calcitonin, and bioactive vitamin D
  • Decreased glomerular filtration, excessive intestinal absorption, dietary supplementation, overuse of phosphate enemas, excessive bone resorption, or significant tissue injury with cell lysis can result in hyperphosphatemia

Systems Affected

General

  • P and Ca2+ metabolism and homeostatic mechanisms are closely linked
  • Hyperphosphatemia frequently occurs with hypocalcemia
  • Metastatic calcification may develop with hyperphosphatemia and concurrent hypercalcemia

Skeletal

In response to hypocalcemia, Ca2+ is mobilized from bone and may lead to abnormal bone formation, bone demineralization, and a skeleton prone to injury.

Endocrine

Hyperphosphatemia stimulates PTH secretion, which causes increased resorption of Ca2+ from bone, kidneys, and intestine and increased renal excretion of P.

Signalment!!navigator!!

  • Any breed, age, or sex
  • Young, growing animals have increased serum P concentrations (4.5–9 mg/dL)

Signs!!navigator!!

General Comments

  • Acute hyperphosphatemia—signs due to concurrent hypocalcemia (e.g. tetany, hyperexcitability, muscle fasciculations arrhythmia, colic)
  • Chronic hyperphosphatemia—lameness, abnormal bone and cartilage development, osteodystrophia fibrosa, fractures

Historical Findings

  • Dependent on the underlying cause
  • Exposure to vitamin D-containing plants
  • High bran diet

Physical Examination Findings

  • Dietary P excess or imbalance—shifting leg lameness, joint pain, or stilted gait; as the disease progresses, abnormal bone formation and enlarged facial bones (e.g. bighead in NHP)
  • Hypervitaminosis D—limb stiffness with painful flexor tendons and suspensory ligaments

Causes and Risk Factors!!navigator!!

  • Young, growing animals—due to rapid bone turnover
  • Decreased glomerular filtration—prerenal, renal (AKI), or postrenal azotemia; chronic renal failure usually is accompanied by hypophosphatemia
  • Hypervitaminosis D—hyperphosphatemia and hypercalcemia result from excessive dietary supplementation with vitamin D-containing products
  • Excessive dietary P or P imbalance—excessive P intake or excessive supplementation with bran, which is high in P, inhibits absorption of Ca2+, resulting in Ca2+ deficiency
  • NHP occurs from excess P and low Ca2+ intake. Secretion of PTH increases to correct the disturbance in mineral homeostasis
  • Hyperphosphatemia from cellular lysis and release of intracellular P can occur with significant tissue injury or necrosis (rhabdomyolysis, tumor necrosis) or hemolysis
  • Increased potential for metastatic calcification with concurrent hyperphosphatemia and hypercalcemia

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

See Causes and Risk Factors.

CBC/Biochemistry/Urinalysis!!navigator!!

  • NHP—normal renal function, hypocalcemia, hyperphosphatemia, elevated ALP concentration
  • Renal disease—azotemia, isosthenuria

Other Laboratory Tests!!navigator!!

  • Dietary deficiency or imbalance—review dietary history, inspect feed, and analyze chemically for Ca2+ and P content
  • NHP—increased urinary P fractional excretion

Imaging!!navigator!!

Radiographs may detect loss of skeletal mineralization when losses >30%.

Treatment ⬆ ⬇

TREATMENT

  • NHP—correction of dietary deficiency or imbalance by supplying the deficient nutrient; dietary Ca2+/P ratio must not exceed 1.5–2:1
  • Removal of vitamin D sources
  • With suspected AKI, fluid replacement and correction of electrolyte imbalances
  • With acute cell lysis or iatrogenic causes, fluid therapy and diuretics

Medications ⬆ ⬇

MEDICATIONS

Drug(s) of Choice

Hypervitaminosis D—removal of source, fluid diuresis, corticosteroid administration, and low Ca2+ and P feeds.

Follow-up ⬆ ⬇

FOLLOW-UP

Expected Course and Prognosis

If soft tissue mineralization in the heart or kidney occurs, prognosis is poor.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

Hypocalcemia

Age-Related Factors!!navigator!!

  • Hyperphosphatemia and elevated ALP activity are common in healthy, young, growing animals
  • Young animals are more prone to skeletal abnormalities resulting from dietary excess or imbalances

Synonyms!!navigator!!

  • Bioactive vitamin D—1,25-dihydroxyvitamin D3, calcitriol
  • Metastatic calcification—soft tissue mineralization
  • NHP—bighead disease, bran disease, osteodystrophia fibrosa

Abbreviations!!navigator!!

  • AKI = acute kidney injury
  • ALP = alkaline phosphatase
  • NHP = nutritional secondary hyperparathyroidism
  • PTH = parathyroid hormone

Suggested Reading ⬆ ⬇

Toribio RE. Phosphorus homeostasis and derangements. In: Fielding CL, Magdesian KG, eds. Equine Fluid Therapy. Ames, IA: Wiley Blackwell, 2015:88–100.

Toribio RE. Parathyroid gland, calcium and phosphorus regulation. In: Smith BP, ed. Large Animal Internal Medicine, 5e. St. Louis, MO: Elsevier Mosby, 2015:1244–1252.

Author(s) ⬆ ⬇

Author: Karen E. Russell

Consulting Editor: Sandra D. Taylor

Additional Further Reading ⬆

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