الفهرس 
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Abstract
Secondary hyperparathyroidism or renal osteodystrophy develops
in most, if not all, Patients with chronic renal failure. chronic
hypocalcaemia is the stimulus resulting in varying degrees of hyperplasia of
parathyroid glands (John et al., 2011).
In chronic renal failure, hypocalcaemia develops because of
phosphate retention and reduced renal synthesis of 1,25 dihydroxy vitamin
D3. Increased PTH secretion is a homeostatic response to hypocalcaemia in
an effort to normalize the serum calcium level by promoting the release of
calcium from bone and indirectly by increasing intestinal absorption of
calcium (Güller and Mayr., 2007).
The results in progressive bone dissolution because of the the action
of PTH on bone. Subsequently, as renal failure progresses.Vitamin D
deficiency develops, alkaline phosphatase level increase, osteitis fibrosa
cystica develops, and serum PTH levels increase further. As the vitamin D
deficiency increases, the intestinal malabsorption of calcium worsens (Pitt
et al., 2009).
Most patients with secondary hyperparathyroidism respond to
medical management; that is directed toward increasing serum calcium and
vitamin D level and deacreasing the serum phosphate level .about 5% to
10% of chronic renal failure patients require parathyroidectomy because of
failed medical management and worsing symptoms or complications (John
et al., 2011)