ISSN 2398-2969      

Renal secondary hyperparathyroidism

icanis

Synonym(s): Rubber jaw, Renal rickets, Renal osteodystrophy


Introduction

  • Excessive production of parathyroid hormone (PTH).
  • Cause: hyperphosphatemia secondary to renal compromise results in formation of complexes with calcium → compensatory increased PTH synthesis. Concurrent deficiency in calcitrol (active vitamin D) is involved in the pathogenesis.
  • Signs: bone pain, signs of renal failure Kidney: chronic kidney disease (CKD).
  • Diagnosis: signs, laboratory tests, radiography.
  • Treatment: manage CRF and attempt to reduce hyperphosphatemia.
  • Prognosis: guarded to poor.

Pathogenesis

Etiology

  • Severe renal dysfunction (congenital > acquired).

Predisposing factors

General
  • Age.

Pathophysiology

  • Reduced glomerular filtration → reduced phosphorus excretion → hyperphosphatemia Hyperphosphatemia → soft tissue mineralization → lowering of [blood calcium].
  • Reduced intestinal absorption of calcium due to defective vitamin D metabolism in CRF → hypocalcemia Hypocalcemia.
  • Hypocalcemia → hypertrophy of parathyroid glands → increased PTH secretion.
  • Decreased active vitamin D → stimulates PTH secretion.
  • PTH → increased osteoclastic activity → bone resorption.

Timecourse

  • Weeks to months.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Cortadellas O, Fernandez del Palacio M T, Talavera J, Bayon A (2010) Calcium and phosphorus homeostasis in dogs with spontaneous chronic kidney disease at different stages of severity. JVIM 24 (1), 73-79 PubMed.
  • Roudebush P, Polzin D J, Adams L G, Towell T L, Forrester S D (2010) An evidence-based review of therapies for canine chronic kidney disease. JSAP 51 (5), 244-252 PubMed.
  • Stillion J R, Ritt M G (2009) Renal secondary hyperparathyroidism in dogs. Compend Contin Educ Vet 31 (6), E8 PubMed.

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