New pathogenic insights inform therapeutic target development for renal osteodystrophy

Research output: Contribution to journalComment/debate

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.

Original languageEnglish
Pages (from-to)261-263
Number of pages3
JournalKidney International
Volume95
Issue number2
DOIs
StatePublished - Feb 2019

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