Chronic Kidney Disease Mineral and Bone DisorderNCT07193056
The CPH-MBD Cohort
An observational study of Chronic Kidney Disease Mineral and Bone Disorder and Chronic Kidney Disease (CKD), run by Herlev Hospital at 1 site in Denmark.
Trial summary
Persons with chronic kidney disease (CKD) have a 3-fold increased risk of bone fracture and a 10-fold increased risk of cardiovascular disease than the general population. These increased risks are related to the disturbances in the mineral metabolism, and this clinical entity is termed Chronic Kidney Disease … Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Chronic Kidney Disease Mineral and Bone Disorder, Chronic Kidney Disease (CKD), Bone Markers
- How many people
- 1,000 participants
- Where
- 1 siteDenmark
- Study dates
- 7 Jan 2026to Jan 2055
- How long will I take part?
- 25 Years
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Participants will be recruited from the outpatient clinic, Department of Nephrology at Herlev Hospital. The outpatient clinic has approximately 1500 patients with CKD4-5nonD.
Who may be able to join
- Age ≥18 years
- CKD stage 4-5nonD (eGFR ≤ 29 ml/min) according to KDIGO (Kidney Disease Improving Global Outcome) definition
Who cannot join
- None
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
Denmark1 site, 1 recruiting
- Recruiting
Department of Nephrology, outpatient clinic, Herlev Hospital
Herlev, 2730
Ditte Hansen, Medical doctor, professor, 004538682877
About this study
Official title: Chronic Kidney Disease -Mineral and Bone Disorder, The CPH-MBD Cohort
Persons with chronic kidney disease (CKD) have a 3-fold increased risk of bone fracture and a 10-fold increased risk of cardiovascular disease than the general population. These increased risks are related to the disturbances in the mineral metabolism, and this clinical entity is termed Chronic Kidney Disease - Mineral and Bone Disorder (CKD-MBD).
The overall aim of the present project is to explore factors that may predict or associate with the development of bone and cardiovascular disease in patients with CKD and hopefully provide insight into underlying mechanisms and pathophysiological pathways for future treatment and prevention.
In a sub study investigators aim to explore the calcium and phosphate balance in patients with CKD and describe how these associate with each other as well as with kidney function (eGFR).
Read the detailed description
Chronic kidney disease (CKD) is a chronic condition where the excretory kidney function (estimated glomerular filtration rate (eGFR)) is reduced and/or markers of kidney damage is present (often presented as albuminuria). CKD is classified into stages CKD G1-5 according the severity of the reduction in eGFR.
The prevalence of CKD is increasing world-wide, partly explained by the increase in the ageing population and prevalence of diabetes3. In Denmark, the prevalence of CKD in the population is 4-8% depending on the applied algorithm. CKD is a devastating disease both due to the risk of kidney failure and thereby the need for dialysis or transplantation, but also because the presence of CKD increases the risk of bone fracture, cardiovascular disease and mortality.
Disturbances in the mineral metabolism, including hyperphosphatemia and hyperparathyroidism develops as kidney function declines. These disturbances are closely related to the increased risk of bone and cardiovascular disease, and this relation has been gathered since 2009 in the clinical entity named Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD).
The bone pathology in patients with CKD, named renal osteodystrophy, can be classified by the TMV classification. The TMV classification describes the bone Turnover, the bone Mineralization and the bone Volume, which may all be disturbed in renal osteodystrophy.
Per see, disturbances in the bone pathology, especially in the bone turnover is considered harmful to the bone strength. However, no studies have addressed if disturbances in the bone turnover increases the risk of bone fracture. This is the primary aim of the present study.
The golden standard for description of bone turnover is a bone biopsy. However, bone turnover markers may describe the bone turnover with a reasonable validity, and will be used in the present study to describe the turnover, as bone biopsy is not considered feasible in 1000 patients.
Especially, the low bone turnover has been a frightened condition as former studies have found an association between low bone turnover and progression of vascular calcification. However, these were executed when treatment with active vitamin D and calcium were more aggressive than today. Treatments that may also affect the vascular calcification. Therefore, it is uncertain if low bone turnover predicts cardiovascular disease. This will also be explored in the present study.
Bone and cardiovascular disease often co-occur in patients with CKD. Preclinical and clinical studies has suggested a bone vascular tissue crosstalk in CKD that may be a mediator of the high risk of fracture and cardiovascular events in patients with CKD. In the present study, it will be possible to explore how these factors, including sclerostin, Dkk-1, and Activin A, associate with changes in bone mineral density (BMD) and future fracture and cardiovascular disease.
Sarcopenia is an age-related disease characterized by a progressive decline in muscle function and mass. Sarcopenia is associated with numerous adverse health outcomes in the general population, including increased risk of falls, fractures, and mortality. Low BMD predicts an increased risk of fracture in the general population as well as in patients with CKD. A few studies have found an association between osteoporosis and sarcopenia in patients with CKD. This association between bone fragility and sarcopenia may be due to common risk factors such as age, sex, and malnutrition, but increasing evidence points towards an interaction between muscles and bone, giving rise to the uniting term osteosarcopenia. The present study will explore if sarcopenia predicts decline in BMD and future fracture.
Patients with CKD are often put on a strict diet to reduce their intake of phosphorous, potassium, sodium and protein. In theory, these dietary restrictions may in turn cause malnutrition, sarcopenia and increased risk of fall and fracture. Especially, the reduced calcium intake due to phosphorous restriction have been speculated to impact on the bone quality. This study will determine the habitual dietary intake of phosphate and calcium in patients with CKD4-5 and explore the association with bone quantity and sarcopenia.
A novel urine acid/base-score (calculated on the basis of urine pH and urine ammonium) assesses the renal tubular capacity for acid excretion and the degree of subclinical acid retention. This disease marker has been found to be largely independent of traditional kidney disease markers and robustly associated with CKD progression and incident ESKD in CKD stage 3-4 patients. This study will determine the association between the subclinical acid retention and clinical outcomes.
The study will include 1000 patients with chronic kidney disease. The patients will be recruited from the outpatient clinic at the Department of Nephrology at Herlev Hospital. The sub study focused on calcium and phosphate balance will include 50 patients with chronic kidney disease.
- Conditions
- Chronic Kidney Disease Mineral and Bone Disorder, Chronic Kidney Disease (CKD), Bone Markers
- Keywords
- bone markers, parathyroid hormone, fracture risk, bone turnover, dietary assessment
- Medical subject headings
- Chronic Kidney Disease-Mineral and Bone Disorder, Renal Insufficiency, Chronic
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| CPH-MBD cohort | Participants will be followed-up for 25 years after inclusion. Bone fractures, cardiovascular events, progression of kidney disease, end-stage kidney disease and death will be collected through linkage with registries during follow-up. There is no intervention in this study. | |
| Detailed dietary assessment | From the CPH-MBD cohort we invite 50 participants to complete a dietary assessment to obtain more accurate information about their calcium and phosphate intake. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Difference in time to first fracture between patients with normal bone turnover and low bone turnover based on bone turnover markers at baseline
Measured: 25 years
Secondary outcomes (7)
Time to fracture
All patients will be followed-up and fractures will be registered
Measured: 25 years
Time to cardiovascular event
All patients will be followed-up and cardiovascular events will be registered
Measured: 25 years
Progression in kidney disease
All patients will be followed-up and kidney function will be registered
Measured: 25 years
Time to end-stage kidney disease
All patients will be followed-up and need for dialysis/kidney transplant will be registered.
Measured: 25 years
Time to death
All patients will be followed-up and death will be registered.
Measured: 25 years
Intake of calcium
Photos of meals and written description
Measured: Daily (for the first three days after inclusion)
Intake of phosphate
Photos of meals and written description
Measured: Daily (for the first three days after inclusion)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Sep 2025
- Study start7 Jan 2026
- Primary completionJan 2055 (estimated)
- Study completionJan 2055 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (21)Papers the sponsor has linked to this study.
- Other trials for Chronic Kidney Disease Mineral and Bone DisorderStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 1,000 participants (estimated)
- Target duration
- 25 Years
Sponsor and investigators
- Lead sponsor
- Herlev Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Freja Stæhr Hassager, Herlev and Gentofte Hospital
- Investigators
- Ditte Hansen, Medical doctor, professor, Study director, Department of Nephrology, Herlev Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07193056
- Sponsor's protocol ID
- H-25039131
- Status last verified
- Sep 2026
- First submitted
- 17 Sep 2025
- Last updated
- 16 Sep 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: We do not plan to share IPD as the trial will be conducted according to local legislation (Databeskyttelsesloven, Databeskyttelsesforordningen and Sundhedsloven), which does not allow sharing data.
Publications
Naylor KL, McArthur E, Leslie WD, Fraser LA, Jamal SA, Cadarette SM, Pouget JG, Lok CE, Hodsman AB, Adachi JD, Garg AX. The three-year incidence of fracture in chronic kidney disease. Kidney Int. 2014 Oct;86(4):810-8. doi: 10.1038/ki.2013.547. Epub 2014 Jan 15.
PubMed 24429401Stevens PE, Levin A; Kidney Disease: Improving Global Outcomes Chronic Kidney Disease Guideline Development Work Group Members. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30. doi: 10.7326/0003-4819-158-11-201306040-00007.
PubMed 23732715Svendsen SL, Rousing AQ, Carlsen RK, Khatir D, Jensen D, Hansen NM, Salomo L, Birn H, Buus NH, Leipziger J, Sorensen MV, Berg P. A Urine pH-Ammonium Acid/Base Score and CKD Progression. J Am Soc Nephrol. 2024 Nov 1;35(11):1533-1545. doi: 10.1681/ASN.0000000000000447. Epub 2024 Jul 17.
PubMed 39485702Evenepoel P, Jorgensen HS, Bover J, Davenport A, Bacchetta J, Haarhaus M, Hansen D, Gracia-Iguacel C, Ketteler M, McAlister L, White E, Mazzaferro S, Vervloet M, Shroff R. Recommended calcium intake in adults and children with chronic kidney disease-a European consensus statement. Nephrol Dial Transplant. 2024 Jan 31;39(2):341-366. doi: 10.1093/ndt/gfad185.
PubMed 37697718Moretti A, Iolascon G. Sclerostin: clinical insights in muscle-bone crosstalk. J Int Med Res. 2023 Aug;51(8):3000605231193293. doi: 10.1177/03000605231193293.
PubMed 37632438Li G, Zhang L, Wang D, AIQudsy L, Jiang JX, Xu H, Shang P. Muscle-bone crosstalk and potential therapies for sarco-osteoporosis. J Cell Biochem. 2019 Sep;120(9):14262-14273. doi: 10.1002/jcb.28946. Epub 2019 May 20.
PubMed 31106446Iwasaki Y, Kazama JJ, Fukagawa M. Molecular Abnormalities Underlying Bone Fragility in Chronic Kidney Disease. Biomed Res Int. 2017;2017:3485785. doi: 10.1155/2017/3485785. Epub 2017 Mar 22.
PubMed 28421193Rashid A, Chaudhary Hauge S, Suetta C, Hansen D. "Sarcopenia and risk of osteoporosis, falls and bone fractures in patients with chronic kidney disease: A systematic review". PLoS One. 2022 Jan 21;17(1):e0262572. doi: 10.1371/journal.pone.0262572. eCollection 2022.
PubMed 35061818Lai S, Muscaritoli M, Andreozzi P, Sgreccia A, De Leo S, Mazzaferro S, Mitterhofer AP, Pasquali M, Protopapa P, Spagnoli A, Amabile MI, Molfino A. Sarcopenia and cardiovascular risk indices in patients with chronic kidney disease on conservative and replacement therapy. Nutrition. 2019 Jun;62:108-114. doi: 10.1016/j.nut.2018.12.005. Epub 2018 Dec 11.
PubMed 30875540Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyere O, Cederholm T, Cooper C, Landi F, Rolland Y, Sayer AA, Schneider SM, Sieber CC, Topinkova E, Vandewoude M, Visser M, Zamboni M; Writing Group for the European Working Group on Sarcopenia in Older People 2 (EWGSOP2), and the Extended Group for EWGSOP2. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019 Jul 1;48(4):601. doi: 10.1093/ageing/afz046. No abstract available.
PubMed 31081853Mace ML, Egstrand S, Morevati M, Olgaard K, Lewin E. New Insights to the Crosstalk between Vascular and Bone Tissue in Chronic Kidney Disease-Mineral and Bone Disorder. Metabolites. 2021 Dec 7;11(12):849. doi: 10.3390/metabo11120849.
PubMed 34940607Mace ML, Gravesen E, Nordholm A, Egstrand S, Morevati M, Olgaard K, Lewin E. The Calcified Vasculature in Chronic Kidney Disease Secretes Factors that Inhibit Bone Mineralization. JBMR Plus. 2022 Mar 1;6(4):e10610. doi: 10.1002/jbm4.10610. eCollection 2022 Apr.
PubMed 35434452Barreto DV, Barreto Fde C, Carvalho AB, Cuppari L, Draibe SA, Dalboni MA, Moyses RM, Neves KR, Jorgetti V, Miname M, Santos RD, Canziani ME. Association of changes in bone remodeling and coronary calcification in hemodialysis patients: a prospective study. Am J Kidney Dis. 2008 Dec;52(6):1139-50. doi: 10.1053/j.ajkd.2008.06.024. Epub 2008 Sep 27.
PubMed 18824289Jorgensen HS, Behets G, Viaene L, Bammens B, Claes K, Meijers B, Naesens M, Sprangers B, Kuypers D, Cavalier E, D'Haese P, Evenepoel P. Diagnostic Accuracy of Noninvasive Bone Turnover Markers in Renal Osteodystrophy. Am J Kidney Dis. 2022 May;79(5):667-676.e1. doi: 10.1053/j.ajkd.2021.07.027. Epub 2021 Oct 26.
PubMed 34710517Salam S, Gallagher O, Gossiel F, Paggiosi M, Khwaja A, Eastell R. Diagnostic Accuracy of Biomarkers and Imaging for Bone Turnover in Renal Osteodystrophy. J Am Soc Nephrol. 2018 May;29(5):1557-1565. doi: 10.1681/ASN.2017050584. Epub 2018 Mar 19.
PubMed 29555831
Study at a glance
From the registry record, last updated by the sponsor on 16 Sep 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Chronic Kidney Disease -Mineral and Bone Disorder, The CPH-MBD Cohort
- ClinicalTrials.gov ID
- NCT07193056
- Acronym / sponsor ID
- H-25039131
- Conditions
- Chronic Kidney Disease Mineral and Bone Disorder, Chronic Kidney Disease (CKD), Bone Markers
- Keywords
- bone markers, parathyroid hormone, fracture risk, bone turnover, dietary assessment
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 1,000 participants (estimated)
- Lead sponsor
- Herlev HospitalUniversity, hospital or other
- Study start
- 7 Jan 2026 (actual)
- Primary completion
- Jan 2055 (estimated)
- Study completion
- Jan 2055 (estimated)
- First posted
- 25 Sep 2025 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Persons with chronic kidney disease (CKD) have a 3-fold increased risk of bone fracture and a 10-fold increased risk of cardiovascular disease than the general population. These increased risks are related to the disturbances in the mineral metabolism, and this clinical entity is termed Chronic Kidney Disease - Mineral and Bone Disorder (CKD-MBD).
The overall aim of the present project is to explore factors that may predict or associate with the development of bone and cardiovascular disease in patients with CKD and hopefully provide insight into underlying mechanisms and pathophysiological pathways for future treatment and prevention.
In a sub study investigators aim to explore the calcium and phosphate balance in patients with CKD and describe how these associate with each other as well as with kidney function (eGFR).
Detailed description
Chronic kidney disease (CKD) is a chronic condition where the excretory kidney function (estimated glomerular filtration rate (eGFR)) is reduced and/or markers of kidney damage is present (often presented as albuminuria). CKD is classified into stages CKD G1-5 according the severity of the reduction in eGFR.
The prevalence of CKD is increasing world-wide, partly explained by the increase in the ageing population and prevalence of diabetes3. In Denmark, the prevalence of CKD in the population is 4-8% depending on the applied algorithm. CKD is a devastating disease both due to the risk of kidney failure and thereby the need for dialysis or transplantation, but also because the presence of CKD increases the risk of bone fracture, cardiovascular disease and mortality.
Disturbances in the mineral metabolism, including hyperphosphatemia and hyperparathyroidism develops as kidney function declines. These disturbances are closely related to the increased risk of bone and cardiovascular disease, and this relation has been gathered since 2009 in the clinical entity named Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD).
The bone pathology in patients with CKD, named renal osteodystrophy, can be classified by the TMV classification. The TMV classification describes the bone Turnover, the bone Mineralization and the bone Volume, which may all be disturbed in renal osteodystrophy.
Per see, disturbances in the bone pathology, especially in the bone turnover is considered harmful to the bone strength. However, no studies have addressed if disturbances in the bone turnover increases the risk of bone fracture. This is the primary aim of the present study.
The golden standard for description of bone turnover is a bone biopsy. However, bone turnover markers may describe the bone turnover with a reasonable validity, and will be used in the present study to describe the turnover, as bone biopsy is not considered feasible in 1000 patients.
Especially, the low bone turnover has been a frightened condition as former studies have found an association between low bone turnover and progression of vascular calcification. However, these were executed when treatment with active vitamin D and calcium were more aggressive than today. Treatments that may also affect the vascular calcification. Therefore, it is uncertain if low bone turnover predicts cardiovascular disease. This will also be explored in the present study.
Bone and cardiovascular disease often co-occur in patients with CKD. Preclinical and clinical studies has suggested a bone vascular tissue crosstalk in CKD that may be a mediator of the high risk of fracture and cardiovascular events in patients with CKD. In the present study, it will be possible to explore how these factors, including sclerostin, Dkk-1, and Activin A, associate with changes in bone mineral density (BMD) and future fracture and cardiovascular disease.
Sarcopenia is an age-related disease characterized by a progressive decline in muscle function and mass. Sarcopenia is associated with numerous adverse health outcomes in the general population, including increased risk of falls, fractures, and mortality. Low BMD predicts an increased risk of fracture in the general population as well as in patients with CKD. A few studies have found an association between osteoporosis and sarcopenia in patients with CKD. This association between bone fragility and sarcopenia may be due to common risk factors such as age, sex, and malnutrition, but increasing evidence points towards an interaction between muscles and bone, giving rise to the uniting term osteosarcopenia. The present study will explore if sarcopenia predicts decline in BMD and future fracture.
Patients with CKD are often put on a strict diet to reduce their intake of phosphorous, potassium, sodium and protein. In theory, these dietary restrictions may in turn cause malnutrition, sarcopenia and increased risk of fall and fracture. Especially, the reduced calcium intake due to phosphorous restriction have been speculated to impact on the bone quality. This study will determine the habitual dietary intake of phosphate and calcium in patients with CKD4-5 and explore the association with bone quantity and sarcopenia.
A novel urine acid/base-score (calculated on the basis of urine pH and urine ammonium) assesses the renal tubular capacity for acid excretion and the degree of subclinical acid retention. This disease marker has been found to be largely independent of traditional kidney disease markers and robustly associated with CKD progression and incident ESKD in CKD stage 3-4 patients. This study will determine the association between the subclinical acid retention and clinical outcomes.
The study will include 1000 patients with chronic kidney disease. The patients will be recruited from the outpatient clinic at the Department of Nephrology at Herlev Hospital. The sub study focused on calcium and phosphate balance will include 50 patients with chronic kidney disease.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Target follow-up
- 25 Years
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| CPH-MBD cohort | – | –Participants will be followed-up for 25 years after inclusion. Bone fractures, cardiovascular events, progression of kidney disease, end-stage kidney disease and death will be collected through linkage with registries during follow-up. There is no intervention in this study. |
| Detailed dietary assessment | – | –From the CPH-MBD cohort we invite 50 participants to complete a dietary assessment to obtain more accurate information about their calcium and phosphate intake. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Participants will be recruited from the outpatient clinic, Department of Nephrology at Herlev Hospital. The outpatient clinic has approximately 1500 patients with CKD4-5nonD.
Key inclusion criteria (2 listed)
- Age ≥18 years
- CKD stage 4-5nonD (eGFR ≤ 29 ml/min) according to KDIGO (Kidney Disease Improving Global Outcome) definition
Key exclusion criteria (1 listed)
- None
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Difference in time to first fracture between patients with normal bone turnover and low bone turnover based on bone turnover markers at baseline
Time frame: 25 years
7 secondary outcomes
Time to fracture
Time frame: 25 years
Time to cardiovascular event
Time frame: 25 years
Progression in kidney disease
Time frame: 25 years
Time to end-stage kidney disease
Time frame: 25 years
Time to death
Time frame: 25 years
Intake of calcium
Time frame: Daily (for the first three days after inclusion)
Intake of phosphate
Time frame: Daily (for the first three days after inclusion)
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 16 Sep 2026.
- Background: PubMed 24429401Naylor KL, McArthur E, Leslie WD, Fraser LA, Jamal SA, Cadarette SM, Pouget JG, Lok CE, Hodsman AB, Adachi JD, Garg AX. The three-year incidence of fracture in chronic kidney disease. Kidney Int. 2014 Oct;86(4):810-8. doi: 10.1038/ki.2013.547. Epub 2014 Jan 15.
- Background: PubMed 23732715Stevens PE, Levin A; Kidney Disease: Improving Global Outcomes Chronic Kidney Disease Guideline Development Work Group Members. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30. doi: 10.7326/0003-4819-158-11-201306040-00007.
- Background: PubMed 39485702Svendsen SL, Rousing AQ, Carlsen RK, Khatir D, Jensen D, Hansen NM, Salomo L, Birn H, Buus NH, Leipziger J, Sorensen MV, Berg P. A Urine pH-Ammonium Acid/Base Score and CKD Progression. J Am Soc Nephrol. 2024 Nov 1;35(11):1533-1545. doi: 10.1681/ASN.0000000000000447. Epub 2024 Jul 17.
- Background: PubMed 37697718Evenepoel P, Jorgensen HS, Bover J, Davenport A, Bacchetta J, Haarhaus M, Hansen D, Gracia-Iguacel C, Ketteler M, McAlister L, White E, Mazzaferro S, Vervloet M, Shroff R. Recommended calcium intake in adults and children with chronic kidney disease-a European consensus statement. Nephrol Dial Transplant. 2024 Jan 31;39(2):341-366. doi: 10.1093/ndt/gfad185.
- Background: PubMed 37632438Moretti A, Iolascon G. Sclerostin: clinical insights in muscle-bone crosstalk. J Int Med Res. 2023 Aug;51(8):3000605231193293. doi: 10.1177/03000605231193293.
- Background: PubMed 31106446Li G, Zhang L, Wang D, AIQudsy L, Jiang JX, Xu H, Shang P. Muscle-bone crosstalk and potential therapies for sarco-osteoporosis. J Cell Biochem. 2019 Sep;120(9):14262-14273. doi: 10.1002/jcb.28946. Epub 2019 May 20.
- Background: PubMed 28421193Iwasaki Y, Kazama JJ, Fukagawa M. Molecular Abnormalities Underlying Bone Fragility in Chronic Kidney Disease. Biomed Res Int. 2017;2017:3485785. doi: 10.1155/2017/3485785. Epub 2017 Mar 22.
- Background: PubMed 35061818Rashid A, Chaudhary Hauge S, Suetta C, Hansen D. "Sarcopenia and risk of osteoporosis, falls and bone fractures in patients with chronic kidney disease: A systematic review". PLoS One. 2022 Jan 21;17(1):e0262572. doi: 10.1371/journal.pone.0262572. eCollection 2022.
- Background: PubMed 30875540Lai S, Muscaritoli M, Andreozzi P, Sgreccia A, De Leo S, Mazzaferro S, Mitterhofer AP, Pasquali M, Protopapa P, Spagnoli A, Amabile MI, Molfino A. Sarcopenia and cardiovascular risk indices in patients with chronic kidney disease on conservative and replacement therapy. Nutrition. 2019 Jun;62:108-114. doi: 10.1016/j.nut.2018.12.005. Epub 2018 Dec 11.
- Background: PubMed 31081853Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyere O, Cederholm T, Cooper C, Landi F, Rolland Y, Sayer AA, Schneider SM, Sieber CC, Topinkova E, Vandewoude M, Visser M, Zamboni M; Writing Group for the European Working Group on Sarcopenia in Older People 2 (EWGSOP2), and the Extended Group for EWGSOP2. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019 Jul 1;48(4):601. doi: 10.1093/ageing/afz046. No abstract available.
- Background: PubMed 34940607Mace ML, Egstrand S, Morevati M, Olgaard K, Lewin E. New Insights to the Crosstalk between Vascular and Bone Tissue in Chronic Kidney Disease-Mineral and Bone Disorder. Metabolites. 2021 Dec 7;11(12):849. doi: 10.3390/metabo11120849.
- Background: PubMed 35434452Mace ML, Gravesen E, Nordholm A, Egstrand S, Morevati M, Olgaard K, Lewin E. The Calcified Vasculature in Chronic Kidney Disease Secretes Factors that Inhibit Bone Mineralization. JBMR Plus. 2022 Mar 1;6(4):e10610. doi: 10.1002/jbm4.10610. eCollection 2022 Apr.
- Individual participant dataSharing planned: No. We do not plan to share IPD as the trial will be conducted according to local legislation (Databeskyttelsesloven, Databeskyttelsesforordningen and Sundhedsloven), which does not allow sharing data.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Ditte Hansen, Medical doctor, professor study director
Department of Nephrology, Herlev Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Chronic Kidney Disease Mineral and Bone Disorder and Chronic Kidney Disease (CKD), run by Herlev Hospital at 1 site in Denmark.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: looking for participants now, as of the sponsor's last update on 16 Sep 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Denmark. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Freja S Hassager, Medical doctor (+4522554707, freja.staehr.hassager.01@regionh.dk), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Difference in time to first fracture between patients with normal bone turnover and low bone turnover based on bone turnover markers at baseline (time frame: 25 years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT07193056, which also lists 21 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 16 Sep 2026; AzTrials last refreshed its copy on 26 Oct 2026.