ArticlePloS one2013
Effects of dietary phosphate on adynamic bone disease in rats with chronic kidney disease--role of sclerostin?
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- Short-term effects of therapeutic diet on bone turnover markers in hemodialysis patients: an exploratory analysis of a randomized crossover trial.Scientific reports · 2026Trial
- Bispecific antibody against sclerostin and DKK1 improves bone health and reduces bone marrow adipose tissue accumulation in experimental chronic kidney disease.Bone research · 2026Article
- Calcium-Based Phosphate Binder Induces Osteomalacia in a Rat Model of Adynamic Bone Disease.Calcified tissue international · 2025Article
- Evaluating Osteoporosis in Chronic Kidney Disease: Both Bone Quantity and Quality Matter.Journal of clinical medicine · 2024Review
- Mild Chronic Kidney Disease Associated with Low Bone Formation and Decrease in Phosphate Transporters and Signaling Pathways Gene Expression.International journal of molecular sciences · 2023Article
- Challenges in establishing animal models for studying osteoimmunology of hypoparathyroidism.Frontiers in veterinary science · 2023Review
- Bone Disease in Chronic Kidney Disease and Kidney Transplant.Nutrients · 2022Review
- The relationship between sclerostin and carotid artery atherosclerosis in patients with stage 3-5 chronic kidney disease.International urology and nephrology · 2020Article
- Transcriptomics: a Solution for Renal Osteodystrophy?Current osteoporosis reports · 2020Review
- High calcium, phosphate and calcitriol supplementation leads to an osteocyte-like phenotype in calcified vessels and bone mineralisation defect in uremic rats.Journal of bone and mineral metabolism · 2019Article
- Elevated levels of serum sclerostin are linked to adverse cardiovascular outcomes in peritoneal dialysis patients.International urology and nephrology · 2018Observational
- Role of the Wnt/International journal of endocrinology · 2018Review
- Adynamic bone disease is a predominant bone pattern in early stages of chronic kidney disease.Journal of nephrology · 2017Review
- Molecular Abnormalities Underlying Bone Fragility in Chronic Kidney Disease.BioMed research international · 2017Review
- From skeletal to cardiovascular disease in 12 steps-the evolution of sclerostin as a major player in CKD-MBD.Pediatric nephrology (Berlin, Germany) · 2016Review
- Article
- Sclerostin and DKK1: new players in renal bone and vascular disease.Kidney international · 2015Review
- Associations between the levels of sclerostin, phosphate, and fibroblast growth factor-23 and treatment with vitamin D in hemodialysis patients with low intact PTH level.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2015Article
- Anti-sclerostin antibody treatment in a rat model of progressive renal osteodystrophy.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High phosphate intake is known to aggravate renal osteodystrophy along various pathogenetic pathways. Recent studies have raised the possibility that dysregulation of the osteocyte Wnt/β-catenin signaling pathway is also involved in chronic kidney disease (CKD)-related bone disease. We investigated the role of dietary phosphate and its possible interaction with this pathway in an experimental model of adynamic bone disease (ABD) in association with CKD and hypoparathyroidism. Partial nephrectomy (Nx) and total parathyroidectomy (PTx) were performed in male Wistar rats. Control rats with normal kidney and parathyroid function underwent sham operations. Rats were divided into three groups and underwent pair-feeding for 8 weeks with diets containing either 0.6% or 1.2% phosphate: sham 0.6%, Nx+PTx 0.6%, and Nx+PTx 1.2%. In the two Nx+PTx groups, serum creatinine increased and blood ionized calcium decreased compared with sham control group. They also presented hyperphosphatemia and reduced serum parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) levels. Fractional urinary excretion of phosphate increased in Nx+PTx 1.2% rats despite lower PTH and FGF23 levels than in sham group. These biochemical changes were accompanied by a decrease in bone formation rates. The Nx+PTx 1.2% group had lower bone volume (BV/TV), higher osteoblast and osteocyte apoptosis, and higher SOST and Dickkopf-1 gene expression than the Nx+PTx 0.6% group. Nx+PTx 0.6% rat had very low serum sclerostin levels, and Nx+PTx 1.2% had intermediate sclerostin levels compared with sham group. Finally, there was a negative correlation between BV/TV and serum sclerostin. These results suggest that high dietary phosphate intake decreases bone volume in an experimental model of CKD-ABD, possibly via changes in SOST expression through a PTH-independent mechanism. These findings could have relevance for the clinical setting of CKD-ABD in patients who low turnover bone disease might be attenuated by optimal control of phosphate intake and/or absorption.
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