New pathogenic insights inform therapeutic target development for renal osteodystrophy.
cross_sectional · Level IV
Where this comes from
- Record sourced from PubMed, PMID 30665565.
- Also identified by DOI 10.1016/j.kint.2018.10.026.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
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.
Medical subject headings
- Chronic Kidney Disease-Mineral and Bone Disorder
- Kidney Failure, Chronic
- Polycystic Kidney, Autosomal Dominant