Secondary hyperparathyroidism in chronic kidney disease: pathomechanism and current treatment possibilities

Endokrynol Pol. 2023;74(5):490-498. doi: 10.5603/ep.95820.

Abstract

Secondary hyperparathyroidism (SHPT) is one of the most common metabolic complications resulting from chronic kidney disease (CKD). The complexity of calcium and phosphate disorders associated with CKD is defined by the Kidney Disease Improvement Global Outcomes (KDIGO) working group as CKD-related mineral and bone disorders (CKD-MBD). The last update of the KDIGO guidelines on the conduct in CKD-MBD was published in 2017. The treatment of SHPT is based on 2 strategies: counteracting hyperphosphataemia and suppressing parathyroid hormone (PTH) secretion. Therapy should be based on optimally selected drugs, taking into account additional effects to reduce the risk of chronic complications and side effects. The creation of new drugs with a better safety profile, significant reduction of side effects, and greater efficiency in achieving target serum phosphorus and PTH values forces the gradual replacement of existing treatment with new pharmacotherapies. The aim of this study is to discuss the latest issues (in connection with the latest KDIGO guidelines) regarding the pathomechanism of secondary hyperparathyroidism and the current directions of the therapy in these disorders.

Keywords: FGF-23; Klotho; calcium and phosphate balance; chronic kidney disease; secondary hyperparathyroidism.

MeSH terms

  • Calcium
  • Chronic Kidney Disease-Mineral and Bone Disorder* / complications
  • Humans
  • Hyperparathyroidism, Secondary* / drug therapy
  • Hyperparathyroidism, Secondary* / etiology
  • Parathyroid Hormone / therapeutic use
  • Renal Insufficiency, Chronic* / complications
  • Renal Insufficiency, Chronic* / therapy

Substances

  • Parathyroid Hormone
  • Calcium