Renal secondary hyperparathyroidism
From Felipedia
Renal secondary hyperparathyroidism is a complication of chronic renal disease characterized by increased endogenous levels of parathyroid gland hormone (PTH). It is more common than primary hyperparathyroidism. In contrast to primary hyperparathyroidism, renal secondary hyperparathyroidism tends not to be autonomous. It is seen frequently in dogs, occasionally in cats, and rarely in other species[1].
With progressive renal disease, serum hyperphosphatemia develops as the glomerular filtration rate decreases. Hyperphosphatemia leads to lower serum concentration of ionized calcium. Renal synthesis of calcitriol is also reduced. Calcitriol normally acts on the intestine and kidneys to maintain normal calcium levels. Decreased ionized calcium and calcitriol concentrations cause an increase in serum PTH concentrations. As glomerular filtration rate decreases with advancing renal disease, PTH concentrations progressively increase, leading to the clinical manifestations of renal secondary hyperparathyroidism.
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Clinical Findings
The predominant signs of renal insufficiency (eg, vomiting, dehydration, polydipsia, polyuria, and depression) are usually present. Skeletal lesions range from minor changes with early (or mild) renal disease to severe fibrous osteodystrophy of advanced renal failure. The volume of affected bones usually is normal (isostotic), particularly in older dogs because of the slow onset of renal failure and lower metabolic activity of bones. Hyperostotic bone lesions, such as facial swelling, may be seen in younger dogs in which deposition of unmineralized osteoid by hyperplastic osteoblasts and production of fibrous connective tissue exceed the rate of bone resorption.
Skeletal involvement is generalized but not uniform. Lesions become apparent earlier and reach a more advanced stage in certain areas, such as cancellous bones of the skull. Resorption of alveolar bone occurs early and results in loose teeth, which may be dislodged easily and interfere with mastication. As a result of accelerated resorption of cancellous bone of the maxilla and mandible, bones become softened and pliable (“rubber jaw” syndrome), and the jaws fail to close properly. This often results in drooling and protrusion of the tongue. Severely demineralized mandibles are predisposed to fractures and displacement of teeth from alveoli. Long bones are less dramatically affected. Lameness, stiff gait, and fractures after minor trauma may result from increased bone resorption.
Lesions
All parathyroid glands are enlarged, initially due to hypertrophy of chief cells and subsequently by compensatory hyperplasia. Although the parathyroids are not autonomous, the concentration of PTH in the peripheral blood often exceeds that of primary hyperparathyroidism. Changes such as osteoclastosis, marrow fibrosis, and a higher concentration of woven osteoid may be seen histologically. Severe hypercalcemia, hyperphosphatemia, and high concentrations of PTH seen in advanced disease may cause osteosclerosis.
Diagnosis
Renal secondary hyperparathyroidism is diagnosed by laboratory abnormalities consistent with renal insufficiency accompanied by an increase in serum PTH. Radioimmunoassay of PTH can be performed at various diagnostic laboratories. Assays that measure fragments of the PTH molecule should not be used because the concentration of biologically inactive metabolites of PTH increases with renal failure.
Treatment
Treatment options include dietary modification, calcitriol supplementation, and phosphate binders, as well as management of the underlying renal disease. Prescription diets with restricted dietary phosphorus are available. Oral calcitriol (1.5-3.5 ng/kg/day) has reversed hyperparathyroidism of chronic renal failure, but calcitriol therapy is contraindicated with hyperphosphatemia or hypercalcemia. (Special compounding of calcitriol is needed because the dosages currently available commercially are much larger than those needed clinically.) Dietary phosphorus binders are used to decrease the amount of phosphorus absorbed in the intestines and should be administered with meals. This therapy is especially important during calcitriol supplementation because calcitriol increases the absorption of phosphorus as well as calcium.
