The pathogenesis of parathyroid gland hyperplasia in chronic renal failure.

A 58-year-old female dialysis patient was admitted to the Nephrology Department at the Hopital Necker because of severe secondary hyperparathyroidism. She had had chronic interstitial nephritis with slowly progressive chronic renal failure for more than 10 years. Intermittent home hemodialysis treatment was started 18 years ago. Symptoms and signs of hyperparathyroidism were present before the patient developed end-stage renal failure, and the severity of osteitis fibrosa progressed despite the initiation of renal replacement therapy. Thirteen years ago, the patient first underwent a surgical neck exploration. One large parathyroid gland weighing 4500 mg was removed. One other gland was identified, which was biopsied and had a normal aspect; it was left in place. The remaining glands could not be identified. Operative and light microscopic findings were compatible with the diagnosis of primary adenoma. The plasma calcium concentration decreased markedly immediately after parathyroidectomy, and radiologic signs of osteitis fibrosa regressed. Severe aluminum intoxication, mainly due to aluminum-contaminated dialysis fluid, was diagnosed 9 years ago. An appropriate dialysis water purification system with reverse osmosis was put in place, and the patient received deferoxamine treatment for several months 8 years ago. Soon thereafter, recurrence of hyperparathyroidism became evident. Several attempts at treating the osteitis fibrosa medically were undertaken, first using calcium carbonate and thereafter small doses of oral 1-alpha cholecalciferol. Several transient hypercalcemic and hyperphosphatemic episodes finally led to cessation of the administration of vitamin D derivatives. Three years ago, the plasma calcium level ranged between 2.5 and 2.7