Background: Most patients with chronic kidney disease (CKD) stage 5 develop secondary hyperparathyroidism (SHPT). SHPT is an adaptive response to CKD and its associated disruptions in the homeostatic control of serum phosphorus, calcium, and vitamin D. The poor control of mineral and parathyroid hormone (PTH) levels characteristic of SHPT is associated with serious clinical consequences.
Objective: This review discusses the pathophysiology and consequences of SHPT, as well as the efficacy and limitations of current treatment modalities.
Methods: Literature searches were conducted using the MEDLINE, EMBASE, and BIOSIS databases. Additional information was obtained from Internet web sites, textbooks, and nephrology congress abstracts.
Results: Patients with uncontrolled SHPT are at higher risk for cardiovascular morbidity and mortality, hospitalization, bone disease, vascular and soft-tissue calcification, and vascular access failure than patients whose mineral and PTH levels are well managed. New National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) targets for calcium, phosphorus, calcium-phosphorus product, and PTH control have recently been published with the aim of improving the management of mineral metabolism in CKD patients. Data from observational studies suggest that the majority of patients currently have PTH and mineral levels outside these target ranges.
Conclusions: Given the inadequacies of current therapies, novel agents are being developed that may help improve the management of SHPT.