ArticlePloS one2017
Circulating levels of sclerostin but not DKK1 associate with laboratory parameters of CKD-MBD.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Lowering of Circulating Sclerostin May Increase Risk of Atherosclerosis and Its Risk Factors: Evidence From a Genome-Wide Association Meta-Analysis Followed by Mendelian Randomization.Arthritis & rheumatology (Hoboken, N.J.) · 2023Pooled it
- Chronic kidney disease: from mineral dysregulation to bone and cardiovascular disease.Journal of endocrinological investigation · 2026Review
- Bispecific antibody against sclerostin and DKK1 improves bone health and reduces bone marrow adipose tissue accumulation in experimental chronic kidney disease.Bone research · 2026Article
- Biochemical bone biomarkers in plasma cell dyscrasias.British journal of haematology · 2026Review
- Markers of Mineral Metabolism in Children With CKD Stages 2 to 5D.Kidney international reports · 2026Article
- Functional Molecular Plasma Biomarkers of Inflammation and Repair in Kidney Disease Progression in Gum Arabica Modality of CKD.International journal of molecular sciences · 2026Article
- Advances in noninvasive diagnosis of renal osteodystrophy.Renal failure · 2025Review
- Hungry Bone Syndrome After Parathyroidectomy for Secondary Hyperparathyroidism: Pathogenesis and Contemporary Clinical Considerations.Journal of clinical medicine · 2025Review
- Plasma Dickkopf-1 Levels Are Associated with Chronic Kidney Disease.Metabolites · 2025Article
- Anemia and Mineral Bone Disorder in Kidney Disease Patients: The Role of FGF-23 and Other Related Factors.International journal of molecular sciences · 2024Review
- Article
- The hidden cross talk between bone and tissues through bone turnover.Advances in laboratory medicine · 2024Article
- Early sclerostin assessment in frail elderly patients with sepsis: insights on short- and long-term mortality prediction.Internal and emergency medicine · 2023Article
- Dickkopf-1 Acts as a Profibrotic Mediator in Progressive Chronic Kidney Disease.International journal of molecular sciences · 2023Article
- Relationships between Circulating Sclerostin, Bone Marrow Adiposity, Other Adipose Deposits and Lean Mass in Post-Menopausal Women.International journal of molecular sciences · 2023Article
- Article
- Updates in the chronic kidney disease-mineral bone disorder show the role of osteocytic proteins, a potential mechanism of the bone-Vascular paradox, a therapeutic target, and a biomarker.Frontiers in physiology · 2023Review
- Exploring the Role of Sclerostin as a Biomarker of Cardiovascular Disease and Mortality: A Scoping Review.International journal of environmental research and public health · 2022Article
- The Calcified Vasculature in Chronic Kidney Disease Secretes Factors that Inhibit Bone Mineralization.JBMR plus · 2022Article
- New Insights to the Crosstalk between Vascular and Bone Tissue in Chronic Kidney Disease-Mineral and Bone Disorder.Metabolites · 2021Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMounting evidence indicates that a disturbed Wnt-β-catenin signaling may be involved in the pathogenesis of chronic kidney disease-mineral and bone and mineral disorder (CKD-MBD). Data on the impact of CKD on circulating levels of the Wnt antagonists sclerostin and Dickkopf related protein 1 (DKK1) and the relationship with laboratory parameters of CKD-MBD are incomplete.
methodsWe analyzed serum sclerostin and DKK1 in 308 patients across the stages of chronic kidney disease (kDOQI stage 1-2 n = 41; CKD stage 3 n = 54; CKD stage 4-5 n = 54; hemodialysis n = 100; peritoneal dialysis n = 59) as well as in 49 healthy controls. We investigated associations with demographics, renal function, parameters of mineral metabolism including 25(OH) vitamin D, 1,25(OH)2 vitamin D, biointact fibroblast growth factor 23 (FGF23), and parathyroid hormone (PTH), and bone turnover markers.
resultsSerum sclerostin, but not DKK1, increases in more advanced stages of CKD and associates with PTH, phosphate, and 1,25(OH)2 vitamin D concentrations. Bone turnover markers are highest in hemodialysis patients presenting the combination of high PTH with low sclerostin level. Serum DKK1 levels are lower in CKD patients than in controls and are not associated with laboratory parameters of mineral metabolism. Interestingly, a direct association between DKK1 and platelet count was observed.
conclusionIn CKD, serum levels of the Wnt inhibitors DKK1 and sclerostin are unrelated, indicating different sites of origin and/ or different regulatory mechanisms. Sclerostin, as opposed to DKK1, may qualify as a biomarker of CKD-MBD, particularly in dialysis patients. DKK1 serum levels, remarkably, correlate almost uniquely with blood platelet counts.
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