الفهرس | Only 14 pages are availabe for public view |
Abstract Secondary hypcrparathyroidisrn is common in patients with chronic renal failure resulting in the development of a variety of clinical complications. Elevated levels of parathyroid hormone occur early in renal insufficiency. The onset of secondary hyper- parathyroidism is the result of altered mineral and hormone metabolism, especially deficiency in active vit. D (calcitriol), as the failing kidney decreases production of this hormone. Since calcitriol is the primary regulator of intestinal calcium uptake, low calcitriol levels can lead to decreased scrum calcium levels. In addition, low calcitriol levels can affect bone mineralization and alter the paratlyroid gland response to calcium, requiring a higher serum calium level to suppress PTH secretion. As kidney function declines, renal excretion of phosphorus also diminishes, increasing serum phosphorus levels. These factor lead both to a rapid release of PTH from the parathyroid gland and secondary hyperparathyroidism. Cardiovascular risk factors are a significant burden in CRF patients. The influence of PTH on myocardial function in RSRD patients is the design of the present study. This study was conducted on forty uraemic patients classified into 2 groups: Group I (not under dialysis) Group II (under regular haemodialysisjand ten normal control persons .(Group III). Thorough history and examination was done, stressing on uraemic complications and absence of exclusion criteria. |