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Chronic Kidney Disease-Mineral and Bone Disorder

Metabolism and Endocrine Disease · NLM MeSH · updated 2026-11-04 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

Decalcification of bone or abnormal bone development due to chronic kidney diseases, in which 1,25-dihydroxyvitamin D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on parathyroid hormone.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

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 (680 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

Decalcification of bone or abnormal bone development due to chronic kidney diseases, in which 1,25-dihydroxyvitamin D3 synthesis by the kidneys is impaired, leading to reduced negative feedback on parathyroid hormone. The resulting secondary hyperparathyroidism eventually leads to bone disorders.

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: Chronic Kidney Disease Mineral and Bone Disorder; CKD-MBD; Renal Rickets; Rickets, Renal; Renal Osteodystrophy; Osteodystrophies, Renal; Renal Osteodystrophies; Osteodystrophy, Renal.

Where it fits in the MeSH classification

Broader topics
Rickets; Kidney Diseases; Hyperparathyroidism, Secondary; Chronic Disease

Related concepts

  • Kidney Diseases
  • Dihydroxyvitamin
  • Parathyroid Hormone
  • Secondary Hyperparathyroidism

Research landscape

PubMed indexes 3,842 records tagged with the MeSH heading “Chronic Kidney Disease-Mineral and Bone Disorder” (counts retrieved 2026-10-31). 360 of them (9.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,263 records.

Reviews account for 972 records (25.3%) and meta-analyses for 22. Randomized controlled trials number 67 (1.7%) 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.

PubMed records by publication periodthrough 1999: 2,263 records; 2000-2009: 641 records; 2010-2019: 578 records; 2020 onward: 360 records2,263through 19996412000-20095782010-20193602020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19992,263
2000-2009641
2010-2019578
2020 onward360
Share of records by publication typeReviews: 25.3 percent; Meta-analyses: 0.6 percent; Randomized controlled trials: 1.7 percentReviews25.3% (972)Meta-analyses0.6% (22)Randomized controlled trials1.7% (67)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 3,842 PubMed records
TypeRecordsShare
Reviews97225.3%
Meta-analyses220.6%
Randomized controlled trials671.7%

Method: PubMed query "Chronic Kidney Disease-Mineral and Bone Disorder"[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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic
Hu L, Napoletano A, Provenzano M, Garofalo C, Bini C, Comai G, et al.
2022Review article
Design not recorded in structured metadata
89cc by
PMID 36293076 · DOI · PMC9603742
Circulating markers of bone turnover
Vervloet MG, Brandenburg VM, CKD-MBD working group of ERA-EDTA
2017Review article
Design not recorded in structured metadata
52cc by
PMID 28502032 · DOI · PMC5628199
Diets for patients with chronic kidney disease, should we reconsider?
Mitch WE, Remuzzi G
2016Research article
Design not recorded in structured metadata
51cc by
PMID 27401192 · DOI · PMC4940838
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
Jørgensen HS, Vervloet M, Cavalier E, Bacchetta J, de Borst MH, Bover J, et al.
2025Research article
Design not recorded in structured metadata
45cc by
PMID 39875204 · DOI · PMC11960744

Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic [1]

Review article Hu L, Napoletano A, Provenzano M, Garofalo C, Bini C, Comai G, et al. · · 2022 · cited 89 times (Europe PMC)

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

Circulating markers of bone turnover [2]

Review article Vervloet MG, Brandenburg VM, CKD-MBD working group of ERA-EDTA · · 2017 · cited 52 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Renal osteodystrophy is a feature of chronic kidney disease (CKD), with increasing prevalence as CKD progresses.
Closing excerpt
This review is based on the overview lecture at the symposium held in Amsterdam, September 23, 2016: "The Bone In CKD", organized by the CKD-MBD working group of ERA-EDTA.
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 (183 words)

Renal osteodystrophy is a feature of chronic kidney disease (CKD), with increasing prevalence as CKD progresses. This bone disease is responsible for major morbidity, including fractures, and a deterioration in the quality of life and its sequelae. Circulating biomarkers of renal osteodystrophy typically indicate bone turnover, but not other features of bone, like bone volume, mineralization, quality or strength. Bone turnover can be considered to be primarily a reflection of bone cell activity, in particular that of osteoblasts and osteoclasts. Since current treatments for bone disease usually target cellular activity, biomarkers are considered to be able to contribute to the decision-making for treatment and its follow-up. In CKD, one has to consider the impact of a diminished clearance of biomarkers or their altered metabolism, both potentially limiting its clinical use. Here, several aspects of the most frequently used biomarkers of bone turnover are reviewed, with an emphasis on the specific situation represented by CKD. This review is based on the overview lecture at the symposium held in Amsterdam, September 23, 2016: "The Bone In CKD", organized by the CKD-MBD working group of ERA-EDTA.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28502032 · DOI · PMC5628199

Diets for patients with chronic kidney disease, should we reconsider? [3]

Research article Mitch WE, Remuzzi G · · 2016 · cited 51 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Here we revisit how dietary factors could affect the treatment of patients with complications of chronic kidney disease (CKD), bringing to the attention of the reader the most recent developments in the field.
Closing excerpt
We will briefly discuss five CKD-induced complications that are substantially improved by dietary manipulation: 1) metabolic acidosis and the progression of CKD; 2) improving the diet to take advantage of the benefits of angiotensin converting enzyme inhibitors (ACEi) on slowing the progression of CKD; 3) the diet and mineral bone disorders in CKD; 4) the safety of nutritional methods utilizing dietary protein restriction; and 5) evidence that new strategies can treat the loss of lean body mass that is commonly present in patients with 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 (118 words)

Here we revisit how dietary factors could affect the treatment of patients with complications of chronic kidney disease (CKD), bringing to the attention of the reader the most recent developments in the field. We will briefly discuss five CKD-induced complications that are substantially improved by dietary manipulation: 1) metabolic acidosis and the progression of CKD; 2) improving the diet to take advantage of the benefits of angiotensin converting enzyme inhibitors (ACEi) on slowing the progression of CKD; 3) the diet and mineral bone disorders in CKD; 4) the safety of nutritional methods utilizing dietary protein restriction; and 5) evidence that new strategies can treat the loss of lean body mass that is commonly present in patients with CKD.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27401192 · DOI · PMC4940838

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 [4]

Research article Jørgensen HS, Vervloet M, Cavalier E, Bacchetta J, de Borst MH, Bover J, et al. · · 2025 · cited 45 times (Europe PMC)

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

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 Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO) [5]
    Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K, et al. · Kidney Int · 2006 · cited 1,299 times (Europe PMC)
  • 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 [6]
    Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, et al. · Kidney Int · 2017 · cited 705 times (Europe PMC)
  • Research article Renal osteodystrophy [7]
    Hruska KA, Teitelbaum SL · N Engl J Med · 1995 · cited 276 times (Europe PMC)
  • Research article Vascular calcification in CKD-MBD: Roles for phosphate, FGF23, and Klotho [8]
    Yamada S, Giachelli CM · Bone · 2017 · cited 254 times (Europe PMC)
  • Research article Chronic kidney disease-mineral-bone disorder: a new paradigm [9]
    Moe SM, Drüeke T, Lameire N, Eknoyan G · Adv Chronic Kidney Dis · 2007 · cited 185 times (Europe PMC)
  • Research article Changing bone patterns with progression of chronic kidney disease [10]
    Drüeke TB, Massy ZA · Kidney Int · 2016 · cited 138 times (Europe PMC)

References

  1. 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
  2. Vervloet MG, Brandenburg VM, CKD-MBD working group of ERA-EDTA. Circulating markers of bone turnover. . 2017. PMID 28502032 · DOI · PMC5628199
  3. Mitch WE, Remuzzi G. Diets for patients with chronic kidney disease, should we reconsider?. . 2016. PMID 27401192 · DOI · PMC4940838
  4. 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
  5. Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K, et al.. Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006. PMID 16641930 · DOI
  6. 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
  7. Hruska KA, Teitelbaum SL. Renal osteodystrophy. N Engl J Med. 1995. PMID 7791820 · DOI
  8. Yamada S, Giachelli CM. Vascular calcification in CKD-MBD: Roles for phosphate, FGF23, and Klotho. Bone. 2017. PMID 27847254 · DOI · PMC5429216
  9. Moe SM, Drüeke T, Lameire N, Eknoyan G. Chronic kidney disease-mineral-bone disorder: a new paradigm. Adv Chronic Kidney Dis. 2007. PMID 17200038 · DOI
  10. Drüeke TB, Massy ZA. Changing bone patterns with progression of chronic kidney disease. Kidney Int. 2016. PMID 26806832 · 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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At a glance

3,842
PubMed records on this heading
9%
published since 2020
972
review articles
67
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

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