ArticleKidney international2018
Impaired osteocyte maturation in the pathogenesis of renal osteodystrophy.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- CALLY index and bone mineral density as risk factors for adjacent vertebral fracture after balloon kyphoplasty for treatment of osteoporotic vertebral compression fracture: a retrospective analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- Chronic kidney disease: from mineral dysregulation to bone and cardiovascular disease.Journal of endocrinological investigation · 2026Review
- Fibroblast growth factor 23 at the crossroads of mineral metabolism and bone disease.Current opinion in nephrology and hypertension · 2026Review
- Impaired bone matrix maturation and mineralization are prevalent in adolescent end-stage kidney disease.JBMR plus · 2026Article
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- The uremic toxin indoxyl sulfate decreases osteocyte RANKL/OPG and increases Wnt inhibitor RNA expression that is reversed by PTH.JBMR plus · 2025Article
- Sclerostin and Wnt Signaling in Idiopathic Juvenile Osteoporosis Using High-Resolution Confocal Microscopy for Three-Dimensional Analyses.Children (Basel, Switzerland) · 2024Article
- Article
- Bone and bone derived factors in kidney disease.Frontiers in physiology · 2024Review
- Extracellular FeScientific reports · 2023Article
- Bone Material Properties in Bone Diseases Affecting Children.Current osteoporosis reports · 2023Review
- Article
- Single cell cortical bone transcriptomics define novel osteolineage gene sets altered in chronic kidney disease.Frontiers in endocrinology · 2023Article
- Novel insights into osteocyte and inter-organ/tissue crosstalk.Frontiers in endocrinology · 2023Review
- Micropetrosis in hemodialysis patients.Bone reports · 2021Article
- Bone marrow adiposity inversely correlates with bone turnover in pediatric renal osteodystrophy.Bone reports · 2021Article
- The Role of DMP1 in CKD-MBD.Current osteoporosis reports · 2021Review
- How FGF23 shapes multiple organs in chronic kidney disease.Molecular and cellular pediatrics · 2021Review
- Vitamin K and D Supplementation and Bone Health in Chronic Kidney Disease-Apart or Together?Nutrients · 2021Review
- Transcriptomics: a Solution for Renal Osteodystrophy?Current osteoporosis reports · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Pediatric renal osteodystrophy is characterized by skeletal mineralization defects, but the role of osteoblast and osteocyte maturation in the pathogenesis of these defects is unknown. We evaluated markers of osteocyte maturation and programmed cell death in iliac crest biopsy samples from pediatric dialysis patients and healthy controls. We evaluated the relationship between numbers of fibroblast growth factor 23 (FGF23)-expressing osteocytes and histomorphometric parameters of skeletal mineralization. We confirmed that chronic kidney disease (CKD) causes intrinsic changes in bone cell maturation using an in vitro model of primary osteoblasts from patients with CKD and healthy controls. FGF23 co-localized with the early osteocyte marker E11/gp38, suggesting that FGF23 is a marker of early osteocyte maturation. Increased numbers of early osteocytes and decreased osteocyte apoptosis characterized CKD bone. Numbers of FGF23-expressing osteocytes were highest in patients with preserved skeletal mineralization indices, and packets of matrix surrounding FGF23-expressing osteocytes appeared to have entered secondary mineralization. Primary osteoblasts from patients with CKD retained impaired maturation and mineralization characteristics in vitro. Addition of FGF23 did not affect primary osteoblast mineralization. Thus, CKD is associated with intrinsic changes in osteoblast and osteocyte maturation, and FGF23 appears to mark a relatively early stage in osteocyte maturation. Improved control of renal osteodystrophy and FGF23 excess will require further investigation into the pathogenesis of CKD-mediated osteoblast and osteocyte maturation failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.