الفهرس 
Anatomy and Embryology of parathyroid glandOnly 14 pages are availabe for public view
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Abstract
Introduction: The annual incidence of end stage renal failure (ESRF) in children population is 8.3 - 12.1 new cases per million. Children with ESRF almost inevitably develop renal hyperparathyroidism (rHPT), subsequently leading to renal osteodystrophy (ROD) and vascular calcifications the major cause of mortality in third decade of life in childhood-onset ESRF. The pathogenesis is complex and remains somewhat enigmatic. Impaired urinary phosphate excretion and hyperphosphatemia, along with decreased activity of renal 1- alpha hydroxylase, which converts 25-hydroxy vitamin D (25 OHD) to 1,25-dihydroxy vitamin D (1,25 (OH)2D) have been implicated in the functional reduction of nephrons in chronic kidney disease (CKD). Aim of the work Aim of the work is to discuss recent trends in surgical management of secondary hyperparathyroidism in children. Summary: Secondary hyperparathyroidism is a common, important and treatable complication of chronic renal failure. Its exact pathogenesis is unknown, but hyperphosphatemia, hypocalcemia, decreased level of 1,25-dihydroxyvitamin D3, decreased expression of calcium and vitamin D receptors and parathyroid hormone resistance may play a role. Longstanding secondary hyperparathyroidism results in osteitis fibrosa cystica (a high turnover bone lesion) and increases the risk of bone pain and fracture. Medical treatment for secondary hyperparathyroidism in patients with chronic renal failure includes treatment with calcium and vitamin D which has been associated with hypercalcemia and hyperphosphatemia. The use of calcimimetics as cinacalcet has been associated with some successs. Cinacalcet targets the calcium sensing receptors and decreases parathyroid hormone level without increasing calcium or phosphorus levels.