Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (747 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Disorders caused by interruption of bone mineralization manifesting as osteomalacia in adults and characteristic deformities in infancy and childhood due to disturbances in normal bone formation. The mineralization process may be interrupted by disruption of vitamin D; phosphorus; or calcium homeostasis, resulting from dietary deficiencies, or acquired, or inherited metabolic, or hormonal disturbances.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Rachitis; Rachitides.
Where it fits in the MeSH classification
- Broader topics
- Bone Diseases, Metabolic; Calcium Metabolism Disorders; Vitamin D Deficiency
- Narrower topics
- Chronic Kidney Disease-Mineral and Bone Disorder; Osteomalacia; Rickets, Hypophosphatemic
- See also
- Genu Valgum; Genu Varum
Related concepts
- Bone Mineralization
- Osteomalacia
- Bone Formation
- Vitamins
- Phosphorus
- Calcium
Research landscape
PubMed indexes 15,061 records tagged with the MeSH heading “Rickets” (counts retrieved 2026-10-31). 1,496 of them (9.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,593 records.
Reviews account for 2,297 records (15.3%) and meta-analyses for 42. Randomized controlled trials number 144 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,593 |
| 2000-2009 | 1,881 |
| 2010-2019 | 2,091 |
| 2020 onward | 1,496 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,297 | 15.3% |
| Meta-analyses | 42 | 0.3% |
| Randomized controlled trials | 144 | 1.0% |
Method: PubMed query "Rickets"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in metabolism and endocrine disease
Studies of diabetes, obesity and hormone disorders often follow blood tests such as glucose, HbA1c or hormone levels, which are stand-ins for outcomes that matter more, such as complications. Lifestyle and diet research is largely observational, and weight and diabetes trials can differ in how long people were followed. Nothing on this page is advice about medicines, insulin or diet; talk to a qualified clinician about your own situation. Check whether the outcome was a lab value or a clinical event, and the type and duration of the condition studied.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic | 2022 | Review article Design not recorded in structured metadata | 89 | cc by PMID 36293076 · DOI · PMC9603742 |
| The role of nutritional vitamin D in chronic kidney disease-mineral and bone disorder in children and adults with chronic kidney disease, on dialysis, and after kidney transplantation-a European consensus statement | 2025 | Research article Design not recorded in structured metadata | 45 | cc by PMID 39875204 · DOI · PMC11960744 |
| Alkaline phosphatase in clinical practice in childhood: Focus on rickets | 2023 | Review article Design not recorded in structured metadata | 38 | cc by PMID 36817604 · DOI · PMC9931734 |
| Hypophosphatemic rickets: diagnosis and treatment | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42138629 · DOI · PMC13178452 |
Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Chronic kidney disease (CKD) is a complex and multifactorial disease, and one of the most prevalent worldwide.
- Closing excerpt
- Lastly, we present specific treatments acting on CKD to prevent and treat the complications associated with secondary hyperparathyroidism (SHPT): control of hyperphosphatemia (with dietary restriction, intestinal phosphate binders, and adequate dialysis), the use of calcimimetic agents, vitamin D, and analogues, and the use of bisphosphonates or denosumab in patients with osteoporosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
Chronic kidney disease (CKD) is a complex and multifactorial disease, and one of the most prevalent worldwide. Chronic kidney disease-mineral bone disorders (CKD-MBD) with biochemical and hormonal alterations are part of the complications associated with the progression of CKD. Pathophysiology of CKD-MBD focused on abnormalities in serum levels of several biomarkers (such as FGF-23, klotho, phosphate, calcium, vitamin D, and PTH) which are discussed in this review. We therefore examine the prognostic association between CKD-MBD and the increased risk for cardiovascular events, mortality, and CKD progression to end-stage kidney disease (ESKD). Lastly, we present specific treatments acting on CKD to prevent and treat the complications associated with secondary hyperparathyroidism (SHPT): control of hyperphosphatemia (with dietary restriction, intestinal phosphate binders, and adequate dialysis), the use of calcimimetic agents, vitamin D, and analogues, and the use of bisphosphonates or denosumab in patients with osteoporosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36293076 · DOI · PMC9603742
The role of nutritional vitamin D in chronic kidney disease-mineral and bone disorder in children and adults with chronic kidney disease, on dialysis, and after kidney transplantation-a European consensus statement [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Vitamin D deficiency is common in patients with chronic kidney disease (CKD) and associates with poor outcomes.
- Closing excerpt
- Future clinical trials should investigate the benefit of vitamin D supplementation on patient-relevant outcomes in the setting of vitamin D deficiency across different stages of CKD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (237 words)
Vitamin D deficiency is common in patients with chronic kidney disease (CKD) and associates with poor outcomes. Current clinical practice guidelines recommend supplementation with nutritional vitamin D as for the general population. However, recent large-scale clinical trials in the general population failed to demonstrate a benefit of vitamin D supplementation on skeletal or non-skeletal outcomes, fueling a debate on the rationale for screening for and correcting vitamin D deficiency, both in non-CKD and CKD populations. In a collaboration between the European Renal Osteodystrophy initiative of the European Renal Association (ERA) and the European Society for Paediatric Nephrology (ESPN), an expert panel performed an extensive literature review and formulated clinical practice points on vitamin D supplementation in children and adults with CKD and after kidney transplantation. These were reviewed by a Delphi panel of members from relevant working groups of the ERA and ESPN. Key clinical practice points include recommendations to monitor for, and correct, vitamin D deficiency in children and adults with CKD and after kidney transplantation, targeting 25-hydroxyvitamin D levels >75 nmol/l (>30 ng/ml). Although vitamin D supplementation appears well-tolerated and safe, it is recommended to avoid mega-doses (≥100 000 IU) and very high levels of 25 hydroxyvitamin D (>150-200 nmol/l, or 60-80 ng/ml) to reduce the risk of toxicity. Future clinical trials should investigate the benefit of vitamin D supplementation on patient-relevant outcomes in the setting of vitamin D deficiency across different stages of CKD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39875204 · DOI · PMC11960744
Alkaline phosphatase in clinical practice in childhood: Focus on rickets [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Serum alkaline phosphatase (ALP) and its isoenzymes reflect bone metabolism: ALP increases the ratio of inorganic phosphate to pyrophosphate systemically and facilitates mineralization as well as reduces extracellular pyrophosphate concentration, an inhibitor of mineral formation.
- Closing excerpt
- Finally, ALP measurements are useful in clinical and therapeutic follow-up.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (248 words)
Serum alkaline phosphatase (ALP) and its isoenzymes reflect bone metabolism: ALP increases the ratio of inorganic phosphate to pyrophosphate systemically and facilitates mineralization as well as reduces extracellular pyrophosphate concentration, an inhibitor of mineral formation. On the contrary, low ALP activity is associated with reduction of bone turnover. ALP includes four isoenzymes depending on the site of tissue expression: intestinal ALP, placental ALP, germ cell ALP and tissue nonspecific ALP or liver/bone/kidney ALP. The bone isoenzyme (B-ALP) is involved in bone calcification and is a marker of bone turnover as a result of osteoblastic activity. ALP and its isoenzymes are crucial in the diagnostic process of all the forms of rickets.The most common cause of rickets is vitamin D nutritional deficiency. The aim of this review is to update on the role played by ALP serum concentrations as a relevant marker in thediagnosis and treatment of rickets. Indeed, the diagnosis of rickets is based on its clinical, radiological and laboratory characteristics. An elevated ALP level is one of the markers for the diagnosis of rickets in children, though it is also associated with bone formation process. ALP is also useful for the differentiation between rickets and other disorders that can mimic rickets because of their clinical and laboratory characteristics, and, together with other biochemical markers, is crucial for the differential diagnosis of the different forms of rickets. Age, severity and duration of rickets may also modulate ALP elevation. Finally, ALP measurements are useful in clinical and therapeutic follow-up.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36817604 · DOI · PMC9931734
Hypophosphatemic rickets: diagnosis and treatment [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Hypophosphatemicrickets (HR) represents a heterogeneous group of disorders characterized by renal phosphate wasting, impaired bone mineralization, and skeletal deformities.
- Closing excerpt
- Advances in understanding these mechanisms have led to the development of targeted therapies, such as burosumab, which are redefining the clinical management of affected individuals.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (120 words)
Hypophosphatemicrickets (HR) represents a heterogeneous group of disorders characterized by renal phosphate wasting, impaired bone mineralization, and skeletal deformities. This narrative review provides an overview of phosphate homeostasis and the molecular mechanisms underlying HR, focusing on the role of Fibroblast Growth Factor 23 (FGF23) in regulating renal phosphate use and vitamin D metabolism. The clinical, biochemical, and genetic features of both FGF23-dependent and -independent forms of HR are discussed, including X-linked hypophosphatemia (XLH), autosomal dominant hypophosphatemic rickets (ADHR), autosomal recessive hypophosphatemic rickets (ARHR), tumor-induced osteomalacia (TIO), hereditary hypophosphatemic rickets with hypercalciuria (HHRH), and Fanconi syndrome. Advances in understanding these mechanisms have led to the development of targeted therapies, such as burosumab, which are redefining the clinical management of affected individuals.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42138629 · DOI · PMC13178452
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters [5]
- Research article Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia [6]
- Research article The health effects of vitamin D supplementation: evidence from human studies [7]
- Research article FGF23 at the crossroads of phosphate, iron economy and erythropoiesis [8]
- Research article Rickets [9]
- Research article Tumor-Induced Osteomalacia [10]
References
- Hu L, Napoletano A, Provenzano M, Garofalo C, Bini C, Comai G, et al.. Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic. . 2022. PMID 36293076 · DOI · PMC9603742
- Jørgensen HS, Vervloet M, Cavalier E, Bacchetta J, de Borst MH, Bover J, et al.. The role of nutritional vitamin D in chronic kidney disease-mineral and bone disorder in children and adults with chronic kidney disease, on dialysis, and after kidney transplantation-a European consensus statement. . 2025. PMID 39875204 · DOI · PMC11960744
- Cannalire G, Pilloni S, Esposito S, Biasucci G, Di Franco A, Street ME. Alkaline phosphatase in clinical practice in childhood: Focus on rickets. . 2023. PMID 36817604 · DOI · PMC9931734
- Bruneau H, Bergwitz C. Hypophosphatemic rickets: diagnosis and treatment. . 2026. PMID 42138629 · DOI · PMC13178452
- Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, et al.. Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters. Kidney Int. 2017. PMID 28646995 · DOI
- Haffner D, Emma F, Eastwood DM, Biosse Duplan M, Bacchetta J, Schnabel D, et al.. Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia. Nat Rev Nephrol. 2019. PMID 31068690 · DOI · PMC7136170
- Bouillon R, Manousaki D, Rosen C, Trajanoska K, Rivadeneira F, Richards JB. The health effects of vitamin D supplementation: evidence from human studies. Nat Rev Endocrinol. 2022. PMID 34815552 · DOI · PMC8609267
- Edmonston D, Wolf M. FGF23 at the crossroads of phosphate, iron economy and erythropoiesis. Nat Rev Nephrol. 2020. PMID 31519999 · DOI
- Carpenter TO, Shaw NJ, Portale AA, Ward LM, Abrams SA, Pettifor JM. Rickets. Nat Rev Dis Primers. 2017. PMID 29265106 · DOI
- Florenzano P, Hartley IR, Jimenez M, Roszko K, Gafni RI, Collins MT. Tumor-Induced Osteomalacia. Calcif Tissue Int. 2021. PMID 32504138 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.