42 - Parathyroidectomy

Abstract

The development of secondary hyperparathyroidism is commonly observed in chronic kidney disease. In these patients, increased parathyroid hormone (PTH) synthesis and secretion, together with elevation of fibroblast growth factor 23 (FGF-23) levels, stimulate phosphaturia to prevent the accumulation of phosphate. In advanced stages of chronic kidney disease, glomerular filtration rates are so low that elevated PTH is not able to prevent the increase in serum phosphate; however, the stimulus for the progressive increase of parathyroid growth is maintained, which may even progress to nodular hyperplasia. Then, parathyroid glands fail to respond to medical therapy, and refractory hyperparathyroidism occurs. Parathyroidectomy (PTX), surgical resection of the parathyroid glands, is usually performed in cases of persistent excessive elevation of serum PTH levels associated with hypercalcemia despite available medical therapy: phosphate binders, active vitamin D, and calcimimetics. PTX can be performed using different procedures: subtotal PTX or total PTX with or without parathyroid autotransplantation. PTH oversuppression is an undesirable consequence of parathyroid surgery, which may cause the development of adynamic bone disease. Hungry bone syndrome is quite common after this surgery. However, if appropriately indicated, PTX improves survival and parameters of mineral metabolism. PTX should be considered in cases of severe hyperparathyroidism that do not respond to pharmacological treatment and with clear undesirable effects of PTH on bone and mineral metabolism.