Secondary hyperparathyroidism (SHPT) is a secondary adaptive response to maintain calcium homeostasis and caused by any condition associated with chronically reduced serum calcium (Ca) levels, and low serum Ca levels lead to compensatory overactivity of the parathyroid gland. It is a common complication of chronic kidney disease (CKD) and is part of the CKD-mineral bone disorder (CKD-MBD). SHPT is associated with increased risk of morbidity and mortality; thus, SHPT control is recommended. SHPT develops in patients with CKD due to a variety of mechanisms including increased phosphorus and fibroblast growth factor 23 (FGF23), and decreased calcium and 1.25-dihydroxyvitamin D levels. Patients present with various bone disorders, cardiovascular disease, and certain patterns of biochemical abnormalities. The diagnosis of patients with SHPT require a combination of clinical investigation and laboratory findings. Many patients with this disease are asymptomatic and only have abnormalities detectable by laboratory and radiologic studies. Laboratory tests may reveal hypocalcemia, normocalcemia or hypercalcemia and hyperphosphatemia. In addition, patients wirh SHPT have extremely elevated parathyroid hormone (PTH) levels, elevated or normal alkaline phosphatase (ALP) levels and decereased vitamin D (vit D) levels. Patients also can become symptomatic. Untreated SHPT leads to progressive bone disease, osteitis fibrosa cystica, and soft tissue calcifications. Patients may experience intractable bone pain, fractures, pruritis, soft tissue or vascular calcifications, calciphylaxis, erythropoietin resistant anemia, and mental status changes.Medical treatment consists of controlling hyperphosphatemia, vit D analogs and Ca administration, and calcimimetic agents. The majority of patients with SHPT can be managed by medical treatment. Despite improvements in medical therapy, it does not always provide control of the SHPT. Some patients require surgical treatment. The surgical indications include PTH levels >500-800 pg/ml associated with hypercalcemia and/or hyperphosphatemia despite medical therapy. Other indications include calciphylaxis, fractures, bone pain or pruritis. Pre-operative imaging is only occasionally helpful except in re-operative parathyroidectomy (PTX). Operative approaches include subtotal PTX, total PTX (TPTX) with or without autotransplantation, and possible thymectomy. Each approach has its own proponents, advantages and disadvantages which are discussed. Hypocalcemia is the most common postoperative complication requiring aggressive calcium administration. Benefits of surgical treatment may include improved survival, bone mineral density and alleviation of symptoms.