Pathophysiology and treatment of secondary hyperparathyroidism in patients with chronic renal failure.
Following four etiologies are considered as the possible reason for secondary hyperparathyroidism in the previous reports. First, a decreased serum concentration of 1,25(OH)2D3 directly stimulates PTH secretion. Second, hypocalcemia directly stimulates PTH secretion which is independent of 1,25(OH)2D3 action. Third, the presence of decreased calcemic response to PTH. Fourth, there is a strong possibility that hyperphosphatemia indirectly and/or directly may stimulate PTH secretion. The treatment of secondary hyperparathyroidism should be modified according to the stage of uremia. Excess suppression of PTH secretion could cause an adynamic bone disease. Early start of the treatment would be beneficial to prevent the bone from the development of PTH resistance.
D000284:Administration, Oral; D000818:Animals; D002117:Calcitriol / Q000627:therapeutic use; D002119:Calcium Carbonate / Q000627:therapeutic use; D004032:Diet; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism / Q000628:therapy; D010281:Parathyroid Hormone / Q000378:metabolism
D010281:Parathyroid Hormone; D002117:Calcitriol; D002119:Calcium Carbonate