Four-Gland Parathyroid Exploration: Subtotal Parathyroidectomy

Hyperparathyroidism is an inevitable feature of end-stage renal disease (ESRD) and is a result of decreased renal tubular excretion of phosphate and defective 1-α hydroxylase enzyme, which cause impaired renal activation of 25-hydroxycholecalciferal to 1,25 dihydroxycholecalciferol. These cause hyperphosphatemia and hypovitaminosis D, which result in prolonged hypocalcemia and lead to hyperplasia of the chief cells of the parathyroid glands and eventually increased secretion of parathyroid hormone (PTH). When the condition is chronic and prolonged, the pathologic changes may become irreversible, with skeletal resistance to PTH and autonomous function of the hyperplastic glands even with correction of the underlying cause and withdrawal of calcium and calcitriol therapy. Parathyroidectomy is usually warranted in severe refractory renal hyperparathyroidism after failure of pharmacologic treatment with calcitriol, a vitamin D analog, or cinacalcet. The procedure is also considered when the medical therapy to reduce the level of intact PTH (iPTH) results in unacceptable elevation of the serum calcium and/or phosphorus (with the potential for precipitation and increased cardiovascular mortality when the calcium-phosphate product exceeds 55 mg²/dl²) or when the adverse effects of the pharmacotherapy are not tolerated by the patient.