In contrast to the intrinsic feedback inhibition defect of primary hyperparathyroidism (HPT), secondary HPT is caused by chronic extrinsic overstimulation of otherwise normal parathyroid glands. This condition is very common in patients with end stage renal disease (ESRD), and secondary HPT develops as a complex sequence of interactions. As the glomerular filtration rate falls, the renal production of 1,23- dihydroxy-vitamin D3 decreases. Moreover, this causes a reduction in intestinal calcium absorption, which creates the parathyroid hormone (PTH) secretion. This secretion increases serum calcium levels by mobilizing calcium from bones. Lastly, the PTH secretion is further stimulated by hyperphosphatemia (via a phosphorous-specific receptor) and a decrease in ionized calcium (from reduced solubility caused by hyperphosphatemia). Intact PTH levels of 500 to 1,500 pg/ml are common (normal: 10~65 pg/ml) in ESRD patients. Long-standing hyperphosphatemia contributes to the alteration of the parathyroid cells, which affect feedback inhibition, due to an increase in ionized calcium. Secondary HPT is mainly controlled by the restriction of phosphate, the inhibition of phosphorous absorption and the supplementation of calcitriol. Secondary HPT, which is unresponsive to medical treatment, it is well known that a total parathyroidectomy and autotransplantation has good results. This report documents our experience with secondary HPT, treated with a total parathyroidectomy and autotransplantation.