ReviewIUBMB life2011
Osteo-renal regulation of systemic phosphate metabolism.
Review in IUBMB life, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Dietary interventions for mineral and bone disorder in people with chronic kidney disease.The Cochrane database of systematic reviews · 2015Pooled it
- Toward improved phosphorus efficiency in monogastrics-interplay of serum, minerals, bone, and immune system after divergent dietary phosphorus supply in swine.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Trial
- Can salivary phosphate levels be an early biomarker to monitor the evolvement of obesity?Contributions to nephrology · 2013Trial
- Interactions between FGF23 and vitamin D.Endocrine connections · 2022Review
- Salivary phosphate as a biomarker for human diseases.FASEB bioAdvances · 2022Article
- Phosphate Burden and Inflammation.Advances in experimental medicine and biology · 2022Article
- Phosphate Dysregulation and Neurocognitive Sequelae.Advances in experimental medicine and biology · 2022Article
- Dietary phosphate toxicity: an emerging global health concern.Histochemistry and cell biology · 2018Review
- Article
- The First Scube3 Mutant Mouse Line with Pleiotropic Phenotypic Alterations.G3 (Bethesda, Md.) · 2016Article
- Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity.BoneKEy reports · 2015Review
- The rachitic tooth.Endocrine reviews · 2014Review
- FGF23 associated bone diseases.Frontiers of medicine · 2013Review
- Inadequate awareness among chronic kidney disease patients regarding food and drinks containing artificially added phosphate.PloS one · 2013Article
- FGF23-induced hypophosphatemia persists in Hyp mice deficient in the WNT coreceptor Lrp6.Contributions to nephrology · 2013Article
- Entpd5 is essential for skeletal mineralization and regulates phosphate homeostasis in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- The role of Klotho in energy metabolism.Nature reviews. Endocrinology · 2012Review
- Can features of phosphate toxicity appear in normophosphatemia?Journal of bone and mineral metabolism · 2012Review
- Genetic induction of phosphate toxicity significantly reduces the survival of hypercholesterolemic obese mice.Biochemical and biophysical research communications · 2011Article
- Dietary and genetic evidence for enhancing glucose metabolism and reducing obesity by inhibiting klotho functions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 2 countries.
Funding
Abstract
Impaired kidney function and subsequent skeletal responses play a critical role in disrupting phosphate balance in chronic kidney disease (CKD) patients with mineral and bone disorder (CKD-MBD). In patients with CKD-MBD, the inability of the kidney to maintain normal mineral ion balance affects bone remodeling to induce skeletal fracture and extraskeletal vascular calcification. In physiological conditions, bone-derived fibroblast growth factor 23 (FGF23) acts on the kidney to reduce serum phosphate and 1,25-dihydroxyvitamin D levels. In humans, increased bioactivity of FGF23 leads to increased urinary phosphate excretion, which induces hypophosphatemic diseases (e.g., rickets/osteomalacia). However, reduced FGF23 activity is associated with hyperphosphatemic diseases (e.g., tumoral calcinosis). In patients with CKD, high serum levels of FGF23 fail to reduce serum phosphate levels and lead to numerous complications, including vascular calcification, one of the important determinants of mortality of CKD-MBD patients. Of particular significance, molecular, biochemical and morphological changes in patients with CKD-MBD are mostly due to osteo-renal dysregulation of mineral ion metabolism. Furthermore, hyperphosphatemia can partly contribute to the development of secondary hyperparathyroidism in patients with CKD-MBD. Relatively new pharmacological agents including sevelamer hydrochloride, calcitriol analogs and cinacalcet hydrochloride are used either alone, or in combination, to minimize hyperphosphatemia and hyperparathyroidism associated complications to improve morbidity and mortality of CKD-MBD patients. This article will briefly summarize how osteo-renal miscommunication can induce phosphate toxicity, resulting in extensive tissue injuries.
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Identifiers
What OpenQuestion holds
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.