Pathogenesis and management of hyperparathyroidism in end‐stage renal disease and after renal transplantation

Abstract

SUMMARY: Secondary hyperparathyroidism is an adaptive response to progressive loss of renal function so as to maintain calcium and phosphate homeostasis, 1,25‐dihydroxyvitamin D3 levels and normal bone turnover, despite skeletal resistance to parathyroid hormone. As feedback regulation fails, complications of parathyroid overactivity develop, and by the commencement of dialysis abnormal bone histology is present in almost all patients, with hyperparathyroid changes most commonly found. Post transplantation, persisting hyperparathyroidism predisposes to osteoporosis. The risk of bone disease is reduced by early, carefully targeted dietary measures and suppressive therapy with calcitriol and calcium‐based phosphate binders, while newer therapies include bisphosphonates and calcimimetics. Timely surgical intervention is necessary in some patients.

Clinical and Radiographic Oral Manifestations in Pediatric Patients with Chronic Renal Failure on Dialysis Therapy

“…We were unable to confirm the effect of secondary hyperparathyroidism and alveolar bone loss observed in adult patients with CRF [22]. In other studies of secondary hyperparathyroidism and bone disease, parathyroid hormone levels seven times higher than the normal upper range [23] have been observed. In this study, 57% of children with CRF had secondary hyperparathyroidism, which revealed a direct relationship between the history of secondary hyperparathyroidism and the signs of osteopenia in children with CRF as determined by the loss of lamina dura and alveolar bone lytic areas.…”