New pathogenic insights inform therapeutic target development for renal osteodystrophy

Kidney Int. 2019 Feb;95(2):261-263. doi: 10.1016/j.kint.2018.10.026.

Abstract

In an ancillary analysis of cross-sectional observational studies of bone health in end-stage kidney disease (ESKD), Evenepoel et al. reported that subjects with autosomal-dominant polycystic kidney disease (ADPKD) had a unique phenotype in their renal osteodystrophy. ADPKD caused resistance to parathyroid hormone (PTH) producing lower turnover states and preservation of cortical bone mineral density. PTH resistance was probably produced by increased osteocyte sclerostin levels, which is regulated by mechanical loading sensed through primary cilia sensory function affected by mutation in PKD1 and PKD2.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Chronic Kidney Disease-Mineral and Bone Disorder*
  • Cross-Sectional Studies
  • Humans
  • Kidney Failure, Chronic*
  • Mutation
  • Phenotype
  • Polycystic Kidney, Autosomal Dominant*
  • TRPP Cation Channels / genetics

Substances

  • TRPP Cation Channels