Secondary hyperparathyroidism is a clinical syndrome in which the parathyroid glands are stimulated by chronic renal failure, intestinal malabsorption syndrome, vitamin D deficiency or resistance to secrete excessive parathyroid hormone due to chronic low blood calcium, low blood magnesium or high blood phosphorus. It occurs in those who have been on hemodialysis for more than 5 years, with an incidence of about 30%. The pathogenesis of parathyroid hyperplasia is due to: 1. Hypocalcemia and hyperphosphatemia due to chronic renal failure, causing compensatory hyperplasia of the parathyroid glands and a state of parathyroid hormone hypersecretion. When the glomerular filtration rate drops to 25 ml/min, the renal excretion of phosphorus decreases and the blood phosphate is retained, which then leads to lower ionized calcium in the extracellular fluid and lower total calcium in the blood. 2, high blood phosphorus can also directly inhibit the renal secretion of 1α-hydroxylase, coupled with the destruction of the kidney tissue itself, so that the production of renal active vitamin D3 is impaired, resulting in reduced intestinal calcium absorption and lower blood calcium. 3, the reduction of active vitamin D3 can make the bone to parathyroid hormone resistance to varying degrees, the parathyroid gland because of the compensatory secretion increased. In renal failure, not only the half-life of parathyroid hormone and its degradation fragments are greatly prolonged, but also the clearance rate of catecholamines and vitamin A is reduced; both catecholamines and vitamin A have the effect of promoting the release of parathyroid hormone. 5, for renal failure with low calcium and low magnesium dialysis solution for dialysis treatment, more likely to aggravate the low blood calcium and resistance to parathyroid hormone and the resulting secondary hyperparathyroidism. Initially, most secondary hyperparathyroidism is treated effectively with medication and symptoms resolve. When the parathyroid glands are stimulated for a long time and form autonomous nodules or adenomas, and when the parathyroid glands are secreting autonomously and are not regulated by blood calcium, it is called triphasic hyperparathyroidism. In this case, drug therapy is not effective, and even after the stimulation of hyperparathyroidism is removed (e.g., kidney transplantation), the symptoms of hyperparathyroidism continue to worsen because the parathyroid glands have developed into functionally autonomous nodular hyperplasia or adenoma, which requires surgical removal to control them.