Parathyroid hormone targets in chronic kidney disease and managing severe hyperparathyroidism

Abstract

Appropriate targets for parathyroid hormone (PTH) in patients with chronic kidney disease (CKD) stages 3–5D are controversial, as are the means by which these targets might be achieved. Secondary hyperparathyroidism is linked to symptoms like bone pain and itch, in addition to less clinically overt issues like bone fragility as well as vascular and soft tissue calcification which may lead to adverse hard endpoints, particularly fracture and death. Recognized therapies for managing a rising PTH include vitamin D analogues, with or without calcimimetic (where available), in addition to management of serum mineral concentrations with diet, binders and dialysis. Despite these interventions, many patients eventually develop refractory metabolic abnormalities of severe hyperparathyroidism (HPT). Treatment decisions in severe HPT in Australia previously centred around whether to perform parathyroidectomy or use calcimimetics in combination with calcitriol (or its analogues) with goals of symptom relief, fracture reduction and reducing vascular risk. The decision to remove Pharmaceutical Benefits Scheme reimbursement for the calcimimetic cinacalcet during 2015, means that parathyroidectomy has now become the only treatment likely to benefit most patients with severe HPT who are medically fit for operative intervention. Although improvements in care are apparent for patients with CKD, there remains an urgent need for basic science and large international trials to inform better ways to manage HPT.