الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Secondary hyperparathyroidism is a major feature of CKD-MBD, secondary hyperparathyroidism occurs in response to a series of abnormalities that initiate and maintain increased parathyroid hormone secretion. These abnormalities include Hypocalcemia, uncontrolled hyperphosphatemia and decreased synthesis of active vitamin D3, together with increased fibroblast growth factor 23 (FGF23) concentration and the reduced expression of vitamin D receptors (VDRs), calcium-sensing receptors (CaSRs) in the parathyroid glands.
Approximately 10 percent of patients with end-stage renal disease (ESRD) undergo parathyroidectomy for secondary hyperparathyroidism. This percentage has remained constant over the past 20 years despite advances in medical therapy.
Delayed or inadequate therapy are thought to be involved in the pathogenesis of refractory hyperparathyroidism, while hyperparathyroidism is associated with increased risk of fractures, cardiovascular morbidity and death, it is important for clinicians to identify and treat those at risk, prevalence of hyperparathyroidism in patients included in our study was 34% in short dialysis vintage patients, and 50% in long dialysis vintage patients.
Considering the multitude of factors that may influence parathyroid gland function, we analyzed the records of ninety chronic maintenance hemodialysis patients who were on hemodialysis for at least 3 months’ duration to identify risk factors predicting or influencing parathyroid hormone secretion.
We investigated the relationship between intact parathyroid hormone and other demographic, clinical and laboratory data to identify possible risk factors associated with hyperparathyroidism.
Serum alkaline phosphatase, phosphorus, calcium phosphate product and serum creatinine were found to be associated with hyperparathyroidism in hemodialysis patients.
Short dialysis vintage patients (dialysis duration <10 years) had the same risk factors of total patient group.
The correlation between intact parathyroid hormone and risk factors identified in the current study were lost in long dialysis vintage patients (dialysis duration >10 years) “except for alkaline phosphatase”, which means that parathyroid gland in long dialysis vintage patients is less responsive to external influences, which may be due to severe or autonomous forms of hyperparathyroidism.
Hyperparathyroidism in long dialysis vintage patients (≥10 years) is negatively correlated with blood pressure and serum sodium level.