Secondary hyperparathyroidism (SHPT) refers to secondary hyperplasia/adenoma formation in parathyroid tissue and elevated serum parathyroid hormone (PTH) levels due to chronic kidney disease. Abnormal calcium and phosphorus metabolism, active vitamin D deficiency, reduced calcium-sensing receptor (CaSR) expression in parathyroid cells, and bone resistance to PTH are all contributing factors. SHPT is mainly seen in patients with chronic renal failure and is an important complication of dialysis treatment in patients with chronic renal failure. Patients with severe SHPT have a significantly reduced quality of life, loss of work capacity, and significantly increased cardiovascular events and all-cause mortality. The pathogenesis of SHPT is associated with low calcium and high phosphorus, active vitamin D deficiency, decreased active vitamin D receptor activity, downregulation of CaSR activator expression and elevated Ca2+ concentration regulating point. long-term stimulation of the parathyroid glands by low calcium and high phosphorus in SHPT patients will lead to diffuse hyperplasia of parathyroid cells and formation of autocrine nodular lesions with enhanced synthesis and secretion of PTH. The clinical features of SHPT manifest as multisystem damage: 1) progressive bone pain, height reduction, pathological fractures, muscle lesions, and periarticular calcification; 2) progressively worsening pruritus, which may present with skin scratching, skin thickening, grayish complexion, and skin calcification; 3) hyperparathyroidism and increased alkaline phosphatase, both of which are elevated at the same time to reflect a state of high bone conversion. If persistent hypercalcemia is present, it suggests the formation of autocrine parathyroid hyperplastic nodules or adenomas; 4. Progressive worsening of renal anemia, leukopenia, platelet insufficiency, and reduced efficacy of erythropoietin therapy; 5. Diffuse bone decalcification or pathological fractures, skeletal deformities, bone fiber cystic changes, sclerosis, etc.; 6. Extraosseous tissues such as calcification, stenosis, and closure insufficiency of heart valves may be present etc. The ideal treatment for SHPT is to block parathyroid hyperplasia, maintain optimal PTH levels and normal physiological concentrations of calcium, maintain normal bone metabolism and prevent vascular calcification. Traditional medical treatment includes phosphorus restriction, phosphorus removal by dialysis, phosphorus binding agents for hyperphosphatemia, maintenance of proper calcium concentration by regulating calcium concentration in dialysis fluid and calcium intake in diet, and inhibition of PTH secretion by applying osteotriol. However, even with a combination of these regimens, some patients with parathyroid hyperplasia progress to nodular hyperplasia and become refractory to SHPT. cinacalcet, a calcium-mimetic compound marketed in the United States in 2004, acts on calcium receptors on the surface of parathyroid cell membranes to divert calcium-mimetic signals, inhibit PTH secretion, and effectively reduce parathyroid cell hyperplasia. cell proliferation and inhibits the development and progression of cardiovascular disease caused by ectopic calcification. The clinical application of cinacalcet had brought great hope to internists that it could reduce the rate of parathyroid surgery and delay the operation time of parathyroidectomy; had a tendency to reduce cardiovascular events and mortality and improve the prognosis; could reduce the risk of fracture and improve the quality of life. However, recent studies have shown that cenacaser is ineffective in the treatment of established parathyroid nodules, is expensive, and requires discontinuation in patients with severe gastrointestinal reactions and rebound from discontinuation. Cinacalcet did not improve all-cause and cardiovascular event mortality in SHPT patients, and the benefit was not significant in SHPT patients. Cenacaser for refractory SHTP is only relevant for those patients who are inoperable. Surgical treatment of refractory SHPT is very safe and effective, providing rapid and significant relief of symptoms (bone pain, muscle weakness, pruritus); rapid reduction of PTH and blood phosphorus, with easy achievement of target values for calcium and phosphorus; improvement of anemia and malnutrition; early surgical treatment to avoid serious complications such as skeletal deformities and fractures; significant reduction in all-cause and cardiovascular event mortality, and improved long-term survival; and superior in efficacy It is by far the most cost-effective treatment for refractory SHTP, especially in terms of lowering PTH and alkaline phosphatase, and is superior to cenacaser in terms of efficacy and cost. There are three main types of SHPT surgery: 1) subtotal parathyroidectomy: after exploring all the glands, only 1/2 or 1/3 of the least hyperplastic glands are preserved and the rest are removed; 2) total parathyroidectomy + autologous transplantation: all the glands are excised and some of the glands are transplanted into the sternocleidomastoid muscle or forearm muscle; 3) total parathyroidectomy: all the glands are excised and no autologous transplantation is performed. Autologous transplantation is not done. Because SHPT is a multi-glandular disease and parathyroid ectopia is more likely, parathyroid hyperplasia in SHPT patients is not reciprocal, and parathyroid glands with insignificant hyperplasia may be powerful, the existing preoperative examination is difficult to locate all parathyroid glands, and the surgeon’s surgical skills and experience are insufficient, traditional total parathyroidectomy may leave parathyroid glands behind and lead to surgical failure or recurrence. The risk of surgical failure or recurrence is high.