Renal secondary hyperparathyroidism (Rubber jaw, Renal rickets, Renal osteodystrophy) Jump to... Pathogenesis Diagnosis Treatment Prevention Sequelae Sources Introduction Excessive production of parathyroid hormone (PTH). Cause : phosphate retention and calcium loss in renal failure  increased PTH synthesis. Signs : pain, facial swelling, signs of renal failure . Diagnosis : signs, laboratory tests, radiography. Treatment : manage CRF and attempt to reduce hyperphosphatemia. Prognosis : guarded to poor. Presenting signs Signs of chronic renal failure  : Polyuria/polydipsia. Anorexia. Weight loss. Lameness/stiffness/bone pain. Pathological fractures. Facial swelling/dysphagia. Age predisposition Young animals with congenital nephropathies. Older animals with chronic renal failure . Breed predisposition Breeds predisposed to congenital renal disease . Pathogenesis Top Etiology Severe renal dysfunction (congenital > acquired). Predisposing factors General Age. Pathophysiology Developing hypocalcemia  increased PTH production  bone resorption. Reduced glomerular filtration  reduced phosphorus excretion  hyperphosphatemia  lowering of [blood calcium]. Reduced gut absorption of calcium due to defective vitamin D metabolism in CRF  hypocalcemia. Hypocalcemia  hypertrophy of parathyroid glands  increased PTH secretion. Decreased active vitamin D  stimulates PTH secretion. PTH  increased osteoclastic activity  bone resorption. Timecourse (incubation, duration) Weeks to months. Diagnosis Top Presenting problems Polyuria/polydipsia. Bone pain/osteopenia. Client history Polyuria/polydipsia. Anorexia. Weight loss. Bone pain. Lameness. Vomiting . Clinical signs Bone/jaw pain. Oral ulceration. Pallor. Diagnostic investigation Biochemistry Urea  and creatinine  elevated. Hyperphosphatemia . Calcium  or ionized calcium  usually low/low normal - total calcium may be elevated/normal/low depending on retention of calcium binding substances but ionized calcium usually low/low normal. ALP  may be increased. PTH  elevated. Must use assay which detects only intact PTH molecule to avoid artefactual elevation in CRF. Radiography Skeletal demineralization particularly of mandibles      'floating teeth'    (increased contrast between teeth and relatively lucent bones). Confirmation of diagnosis Discriminatory diagnostic features Clinical signs. Laboratory tests. Radiography. Definitive diagnostic features PTH assay. Gross autopsy findings Fibrous osteodystrophy, eg flexible ribs, flexible mandible and maxillae (rubber jaw), thinning of long bone cortex, possible bone deformities or pathological fractures. Signs of renal disease, eg kidneys shrunken, with irregular outline   . Enlarged parathyroid glands. Histopathology findings Hyperplasia of parathyroids. Metastatic soft tissue calcification, eg arteries, kidneys, lungs. Osteomalacia. Renal disease, eg end stage kidney, fibrosis, inflammation. Differential diagnosis Primary hyperparathyroidism . Nutritional secondary hyperparathyroidism . Hypovitaminosis D. Treatment Top Initial symptomatic treatment Reduction of hyperphosphatemia Dietary phosphate restriction. Phosphate binders  (calcium hydroxide) or preferably aluminium salts (50-100 mg/kg/day) as this will not cause hypercalcemia. Tend to be impalatable Calcitriol therapy (1.5-6.5 ng/kg/day) starting with a low dose increasing as required. Use only if hyperphosphatemia is controlled. Subsequent management Monitoring Serial measurements of PTH  after 1 and 4 weeks then 3 monthly intervals to indicate effectiveness of phosphate reduction therapy. Renal function. [Serum calcium]. Sequelae Top Prognosis Guarded, animals with renal secondary hyperparathyroidism have severe renal disease. Expected response to treatment Reducing PTH and phosphate levels. Reasons for treatment failure Inadequate treatment of hyperphosphatemia. Progressive renal failure. In hypercalcemic animals with CRF - incorrect diagnosis, ie primary hyperparathyroidism  or hypercalcemia related to malignancy. Sources Top Publications Refereed papers Recent references from PubMed. Nagode L A, Chew D J & Podell M (1996) Benefits of calcitriol therapy and serum phosphorus control in dogs and cats with chronic renal failure. Vet Clin North Am Small Anim Practice 26 , 1293-1330. Yaphe W & Forrester S D (1994) Renal secondary hyperparathyroidism - pathophysiology, diagnosis and treatment. Comp Cont Ed Vet 16 , 173-181. Vetstream contributor(s) Dr Phil Nicholls BVSc BSc PhD MRCVS , Royal Veterinary College, Royal College Street, London NW1 0TU, UK. Dr Melissa S Wallace DVM DipACVIM , Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive West, Madison, WI 53706-8020, USA. Back to top © Copyright Vetstream CANIS DIS02415

Subscribers and trialists can view the additional links below and within theadjacent article. To trial our services click here: Aluminum antacid Bladder: neoplasia Blood biochemistry: alkaline phosphatase (ALP) Blood biochemistry: creatinine Blood biochemistry: ionized calcium Blood biochemistry: phosphate Blood biochemistry: total calcium Blood biochemistry: urea Chronic renal failure Hyperparathyroidism (primary) Juvenile renal disease Nutritional secondary hyperparathyroidism PTH assay Radiography: skull (basic) Radiology: appendicular skeleton (long bones) Renal function assessment Uremia Urolithiasis Vomiting Please click on the links below to view this months other FOC content: Hyperparathyroidism (primary) Primary hypoparathyroidism PTH assay

Copyright © Vetstream  Terms and Conditions  Privacy policy