RENAL SECONDARY HYPERPARATHYROIDISM - PATHOPHYSIOLOGY, DIAGNOSIS, ANDTREATMENT

Renal secondary hyperparathyroidism results from alterations in minera l homeostasis associate wit renal dysfunction. Loss of nephrons and re duction in glomerular filtration rate promote phosphorus retention tha t in turn, causes decreased ionized calcium concentrations and calcitr iol production. Availability of calcitriol is further diminished by re duced renal synthetic capability. Renal secondary hyperparathyroidism occurs as increased amounts of parathyroid hormone are needed to maint ain the calcium-phosphorus balance. In human and animal models, clinic al manifestations of renal secondary hyperparathyroidism can include o steodystrophy, soft tissue mineralization, anemia, glucose intolerance , neurologic abnormalities, and pruritus. Previous parathyroid hormone assays have detected immunoreactive but biologically inactive parathy roid hormone fragments. Recently, an assay that detects only the bioac tive intact parathyroid hormone molecule has been validated in dogs. T reatment options for the management of renal secondary hyperparathyroi dism include dietary modification, intestinal phosphate binders, calci triol, and parathyroidectomy.