<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT02999204</url>
  </required_header>
  <id_info>
    <org_study_id>#10-010</org_study_id>
    <nct_id>NCT02999204</nct_id>
  </id_info>
  <brief_title>Effect of Vitamin D3 Supplementation on Arterial and Bone Remodeling in Chronic Kidney Disease Patients</brief_title>
  <official_title>Effect of Vitamin D3 Supplementation on Arterial and Bone Remodeling in Chronic Kidney Disease Patients</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Jewish General Hospital</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Jewish General Hospital</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      To evaluate in patients with chronic kidney disease the impact of two dosages of per os&#xD;
      vitamin D3 supplementation (cholecalciferol) on large arterial stiffness (evaluated non&#xD;
      invasively by pulse wave velocity and high-resolution echotracking system). We will also&#xD;
      study arterial calcification (lateral abdominal radiography and echocardiogram), arterial&#xD;
      remodeling (high-resolution echotracking system), endothelial function (evaluated by a&#xD;
      non-invasive finger biosensor device), and bone remodeling (evaluated by serum biomarkers and&#xD;
      bone mineral density).&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Structural changes to large arteries and abnormalities in mineral and bone metabolism are&#xD;
      frequent manifestations in patients with chronic kidney disease (CKD). Together, they&#xD;
      contribute in a large part to the heightened morbidity and mortality observed in this&#xD;
      population.&#xD;
&#xD;
      Epidemiological data in end stage renal disease and in the general population suggest the&#xD;
      existence of a bone-vascular axis. Metabolic bone disease (MBD) in CKD encompasses altered&#xD;
      bone remodeling and the propensity for vascular calcification. These pathological processes&#xD;
      are driven by the multiple disorders of mineral metabolism in CKD, among them, abnormalities&#xD;
      of vitamin D metabolism.&#xD;
&#xD;
      Vitamin D deficiency [25(OH)D] is widely observed in CKD patients and has been associated&#xD;
      with an increased rate of cardiovascular events in both the general population and in CKD&#xD;
      patients. The mechanisms involved are not clearly established. Vitamin D influences blood&#xD;
      pressure through effects on the renin-angiotensin system (via a vitamin D response element in&#xD;
      the renin gene), vascular smooth muscle cells and cardiomyocyte proliferation and&#xD;
      hypertrophy, vascular inflammation and calcification. Vitamin D deficiency has been&#xD;
      associated with large arterial stiffness in end-stage renal disease patients. Aortic and&#xD;
      carotid stiffness are independent predictors of cardiovascular and overall mortality in&#xD;
      end-stage renal disease patients. Large arterial remodeling and stiffening could be the&#xD;
      missing pathogenic link between vitamin D deficiency and increased cardiovascular event rate.&#xD;
&#xD;
      In terms of mineral metabolism, many CKD patients develop secondary hyperparathyroidism. This&#xD;
      results from a combination of hyperphosphatemia, hypocalcemia and low levels of active&#xD;
      Vitamin D [1,25(OH)D2]. Since several observational studies have shown that parathyroid&#xD;
      hormone (PTH) levels are inversely correlated with blood 25(OH)D levels, it is possible that&#xD;
      25(OH)D deficiency may also be contributing to the hyperparathyroid state. Secondary&#xD;
      hyperparathyroidism contributes to cardiovascular risk and to bone disease. Elevated PTH has&#xD;
      been associated with large arterial stiffness and remodeling. Elevated PTH is also associated&#xD;
      with high bone turnover and participates in the development of bone disease of CKD-MBD. Bone&#xD;
      disease in CKD-MBD comprises abnormalities in bone turnover, mineralization, linear growth&#xD;
      and strength. Bone biopsy remains the gold standard for evaluation of bone disease in CKD but&#xD;
      its invasive nature limits its practice. Serum biomarkers of bone remodeling allow direct&#xD;
      estimation of bone remodeling but lack evaluation and precision. Among them, guidelines&#xD;
      issued by Kidney Disease Improving Global Outcomes (KDIGO) recommend PTH (1-84) and bone&#xD;
      specific alkaline phosphatase (BSALP). Other biomarkers exist including osteocalcin,&#xD;
      osteoprotegerin, tartrate-resistant acid phosphate-5b (TRAP-5b), pyridinoline and&#xD;
      deoxypyridinoline, procollagen type 1 amino-terminal extension peptides, C terminal&#xD;
      cross-link (CTX) , FGF-23 and fetuin-A. The major limitation of the use of these biomarkers&#xD;
      is their kidney-dependent elimination that affects their measured levels depending on the&#xD;
      degree of kidney dysfunction. We have chosen to study, in addition to PTH (1-84) and BSALP,&#xD;
      CTX, osteoprotegerin, osteocalcin, fetuin-A and fibroblast growth factor-23 (FGF-23) because&#xD;
      a relationship between these biomarkers and arterial disease has never been demonstrated.&#xD;
&#xD;
      This study seeks to compare the impact of standard versus aggressive Vitamin D3&#xD;
      supplementation (in Vitamin D deficient CKD patients) on important vascular and bone health&#xD;
      endpoints.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date type="Actual">January 2015</start_date>
  <completion_date type="Actual">October 1, 2020</completion_date>
  <primary_completion_date type="Actual">September 23, 2020</primary_completion_date>
  <phase>Phase 4</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>Randomized</allocation>
    <intervention_model>Parallel Assignment</intervention_model>
    <primary_purpose>Treatment</primary_purpose>
    <masking>Double (Participant, Care Provider)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>Aortic stiffness evaluated by pulse wave velocity (PWV) (Sphygmocor ® )</measure>
    <time_frame>12 months</time_frame>
    <description>Parameter measured in meters per second.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Carotid stiffness evaluated by high resolution echotracking system (Art-lab®).</measure>
    <time_frame>12 months</time_frame>
    <description>Parameter measured as the difference in millimeters in carotid artery diameter between systole and diastole.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Endothelial function evaluated by Endo-PAT2000® system</measure>
    <time_frame>12 months</time_frame>
    <description>Parameter measured as the reactive hyperemia index as calculated by the Endo-PAT2000® system software.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Aortic valve calcification obtained from echocardiography.</measure>
    <time_frame>12 months</time_frame>
    <description>Parameter measured using a semi-quantitative scoring system based on scale of 1-4 as described by Rosenhek et al, New England Journal of Medicine 2000;343 (9):611.&#xD;
1-no calcification, 2-mildly calcified (small isolated spots), 3-moderately calcified (multiple larger spots), 4-heavily calcified (extensive thickening and calcification of all cusps).</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Calcification of the aorta obtained by plain lateral radiography.</measure>
    <time_frame>12 months</time_frame>
    <description>Parameter measured using a semi-quantitative scoring system based on a scale of 0-3 as described by Kauppila et al, Atherosclerosis 1997;132:245.&#xD;
0-no calcification, 1-small scattered calcific deposits filling less than 1/3 of the longitudinal wall of the aorta, 2-one third or more, but less than two thirds of the longitudinal wall of the aorta calcified, 3-two thirds or more of the longitudinal wall of the aorta calcified.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Bone mineral density</measure>
    <time_frame>12 months</time_frame>
    <description>Osteodensitometry of the lumbar spine, hip, and distal radius, using dual-energy X-ray absorptiometry and reported in grams per square centimeter.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Parathyroid hormone levels</measure>
    <time_frame>12 months</time_frame>
    <description>Measurement of parathyroid hormone levels using a commercially available intact parathyroid hormone ELISA kit with values reported in ng/L.</description>
  </secondary_outcome>
  <number_of_arms>2</number_of_arms>
  <enrollment type="Actual">57</enrollment>
  <condition>Renal Insufficiency, Chronic</condition>
  <condition>Vascular Stiffness</condition>
  <condition>Bone Diseases, Metabolic</condition>
  <arm_group>
    <arm_group_label>Vitamin D3 5,000 units per week</arm_group_label>
    <arm_group_type>Active Comparator</arm_group_type>
    <description>Patient receive a dose that is considered within the standard dosing range for Vitamin D3 for one year.</description>
  </arm_group>
  <arm_group>
    <arm_group_label>Vitamin D3 50,000 units per week</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>Patients receive a more aggressive Vitamin D3 dosing regimen of 50,000 units weekly for the first 3 months. At this point Vitamin D3 levels are measured. If the patient is Vitamin D3 replete (&gt;75 nmol/L) then the dose is reduced to the equivalent of 25,000 units per week for the next 9 months. If the level is below this threshold then 50,000 units per week is continued for the next 9 months</description>
  </arm_group>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Vitamin D3</intervention_name>
    <description>Two different doses of Vitamin D3</description>
    <arm_group_label>Vitamin D3 5,000 units per week</arm_group_label>
    <arm_group_label>Vitamin D3 50,000 units per week</arm_group_label>
    <other_name>cholecalciferol</other_name>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Patients with CKD stage 3-4 [estimated glomerular filtration rate (GFR) by&#xD;
             modification of diet in renal disease (MDRD) formula between 15 and 60 ml/min/1.73m2].&#xD;
&#xD;
          -  Serum vitamin D level&lt;50 nmol/L.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Patient with estimated GFR by MDRD formula below 15 or above 60 ml/min/1.73m2).&#xD;
&#xD;
          -  Serum vitamin D level &gt;50 nmol/L.&#xD;
&#xD;
          -  Liver disease manifested by elevated alanine aminotransferase (ALT) more than 3 times&#xD;
             the upper limit of normal reference range, elevated gamma-glutamyl transferase (GGT)&#xD;
             and total bilirubin levels.&#xD;
&#xD;
          -  History of malabsorption or chronic diarrhea.&#xD;
&#xD;
          -  Patients on biphosphonates, estrogen replacement therapy, PTH analogs,&#xD;
             glucocorticosteroids, calcimimetics, and active vitamin D [1,25(OH)].&#xD;
&#xD;
          -  Patients on antiepileptic medications or other medications affecting vitamin D&#xD;
             metabolism (e.g. phenobarbital, phenytoin, rifampicin).&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>75 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Mark L Lipman, M.D.</last_name>
    <role>Principal Investigator</role>
    <affiliation>Jewish General Hospital</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>Jewish General Hospital</name>
      <address>
        <city>Montreal</city>
        <state>Quebec</state>
        <zip>H3T1E2</zip>
        <country>Canada</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Canada</country>
  </location_countries>
  <results_reference>
    <citation>Guerin AP, Blacher J, Pannier B, Marchais SJ, Safar ME, London GM. Impact of aortic stiffness attenuation on survival of patients in end-stage renal failure. Circulation. 2001 Feb 20;103(7):987-92. doi: 10.1161/01.cir.103.7.987.</citation>
    <PMID>11181474</PMID>
  </results_reference>
  <results_reference>
    <citation>London GM, Guerin AP, Verbeke FH, Pannier B, Boutouyrie P, Marchais SJ, Metivier F. Mineral metabolism and arterial functions in end-stage renal disease: potential role of 25-hydroxyvitamin D deficiency. J Am Soc Nephrol. 2007 Feb;18(2):613-20. doi: 10.1681/ASN.2006060573. Epub 2007 Jan 3.</citation>
    <PMID>17202417</PMID>
  </results_reference>
  <results_reference>
    <citation>Kendrick J, Targher G, Smits G, Chonchol M. 25-Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. Atherosclerosis. 2009 Jul;205(1):255-60. doi: 10.1016/j.atherosclerosis.2008.10.033. Epub 2008 Nov 11.</citation>
    <PMID>19091317</PMID>
  </results_reference>
  <results_reference>
    <citation>Motiwala SR, Wang TJ. Vitamin D and cardiovascular disease. Curr Opin Nephrol Hypertens. 2011 Jul;20(4):345-53. doi: 10.1097/MNH.0b013e3283474985.</citation>
    <PMID>21519252</PMID>
  </results_reference>
  <results_reference>
    <citation>Artaza JN, Mehrotra R, Norris KC. Vitamin D and the cardiovascular system. Clin J Am Soc Nephrol. 2009 Sep;4(9):1515-22. doi: 10.2215/CJN.02260409. Epub 2009 Aug 20.</citation>
    <PMID>19696220</PMID>
  </results_reference>
  <results_reference>
    <citation>Barreto DV, Barreto FC, Liabeuf S, Temmar M, Boitte F, Choukroun G, Fournier A, Massy ZA. Vitamin D affects survival independently of vascular calcification in chronic kidney disease. Clin J Am Soc Nephrol. 2009 Jun;4(6):1128-35. doi: 10.2215/CJN.00260109. Epub 2009 May 14.</citation>
    <PMID>19443628</PMID>
  </results_reference>
  <verification_date>February 2021</verification_date>
  <study_first_submitted>August 29, 2016</study_first_submitted>
  <study_first_submitted_qc>December 16, 2016</study_first_submitted_qc>
  <study_first_posted type="Estimate">December 21, 2016</study_first_posted>
  <last_update_submitted>February 12, 2021</last_update_submitted>
  <last_update_submitted_qc>February 12, 2021</last_update_submitted_qc>
  <last_update_posted type="Actual">February 16, 2021</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>Jewish General Hospital</investigator_affiliation>
    <investigator_full_name>Mark L. Lipman</investigator_full_name>
    <investigator_title>Associate Professor of Medicine</investigator_title>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Bone Diseases</mesh_term>
    <mesh_term>Bone Diseases, Metabolic</mesh_term>
    <mesh_term>Kidney Diseases</mesh_term>
    <mesh_term>Renal Insufficiency, Chronic</mesh_term>
    <mesh_term>Renal Insufficiency</mesh_term>
    <mesh_term>Metabolic Diseases</mesh_term>
  </condition_browse>
  <intervention_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Vitamin D</mesh_term>
    <mesh_term>Cholecalciferol</mesh_term>
  </intervention_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT02999204
org study id: #10-010
nct id: NCT02999204
lead sponsor: 
has dmc: No
To evaluate in patients with chronic kidney disease the impact of two dosages of per os
      vitamin D3 supplementation (cholecalciferol) on large arterial stiffness (evaluated non
      invasively by pulse wave velocity and high-resolution echotracking system). We will also
      study arterial calcification (lateral abdominal radiography and echocardiogram), arterial
      remodeling (high-resolution echotracking system), endothelial function (evaluated by a
      non-invasive finger biosensor device), and bone remodeling (evaluated by serum biomarkers and
      bone mineral density).
Structural changes to large arteries and abnormalities in mineral and bone metabolism are
      frequent manifestations in patients with chronic kidney disease (CKD). Together, they
      contribute in a large part to the heightened morbidity and mortality observed in this
      population.

      Epidemiological data in end stage renal disease and in the general population suggest the
      existence of a bone-vascular axis. Metabolic bone disease (MBD) in CKD encompasses altered
      bone remodeling and the propensity for vascular calcification. These pathological processes
      are driven by the multiple disorders of mineral metabolism in CKD, among them, abnormalities
      of vitamin D metabolism.

      Vitamin D deficiency [25(OH)D] is widely observed in CKD patients and has been associated
      with an increased rate of cardiovascular events in both the general population and in CKD
      patients. The mechanisms involved are not clearly established. Vitamin D influences blood
      pressure through effects on the renin-angiotensin system (via a vitamin D response element in
      the renin gene), vascular smooth muscle cells and cardiomyocyte proliferation and
      hypertrophy, vascular inflammation and calcification. Vitamin D deficiency has been
      associated with large arterial stiffness in end-stage renal disease patients. Aortic and
      carotid stiffness are independent predictors of cardiovascular and overall mortality in
      end-stage renal disease patients. Large arterial remodeling and stiffening could be the
      missing pathogenic link between vitamin D deficiency and increased cardiovascular event rate.

      In terms of mineral metabolism, many CKD patients develop secondary hyperparathyroidism. This
      results from a combination of hyperphosphatemia, hypocalcemia and low levels of active
      Vitamin D [1,25(OH)D2]. Since several observational studies have shown that parathyroid
      hormone (PTH) levels are inversely correlated with blood 25(OH)D levels, it is possible that
      25(OH)D deficiency may also be contributing to the hyperparathyroid state. Secondary
      hyperparathyroidism contributes to cardiovascular risk and to bone disease. Elevated PTH has
      been associated with large arterial stiffness and remodeling. Elevated PTH is also associated
      with high bone turnover and participates in the development of bone disease of CKD-MBD. Bone
      disease in CKD-MBD comprises abnormalities in bone turnover, mineralization, linear growth
      and strength. Bone biopsy remains the gold standard for evaluation of bone disease in CKD but
      its invasive nature limits its practice. Serum biomarkers of bone remodeling allow direct
      estimation of bone remodeling but lack evaluation and precision. Among them, guidelines
      issued by Kidney Disease Improving Global Outcomes (KDIGO) recommend PTH (1-84) and bone
      specific alkaline phosphatase (BSALP). Other biomarkers exist including osteocalcin,
      osteoprotegerin, tartrate-resistant acid phosphate-5b (TRAP-5b), pyridinoline and
      deoxypyridinoline, procollagen type 1 amino-terminal extension peptides, C terminal
      cross-link (CTX) , FGF-23 and fetuin-A. The major limitation of the use of these biomarkers
      is their kidney-dependent elimination that affects their measured levels depending on the
      degree of kidney dysfunction. We have chosen to study, in addition to PTH (1-84) and BSALP,
      CTX, osteoprotegerin, osteocalcin, fetuin-A and fibroblast growth factor-23 (FGF-23) because
      a relationship between these biomarkers and arterial disease has never been demonstrated.

      This study seeks to compare the impact of standard versus aggressive Vitamin D3
      supplementation (in Vitamin D deficient CKD patients) on important vascular and bone health
      endpoints.
allocation: Randomized
intervention model: Parallel Assignment
primary purpose: Treatment
masking: Double (Participant, Care Provider)
measure: Aortic stiffness evaluated by pulse wave velocity (PWV) (Sphygmocor ® )
time frame: 12 months
description: Parameter measured in meters per second.
measure: Carotid stiffness evaluated by high resolution echotracking system (Art-lab®).
time frame: 12 months
description: Parameter measured as the difference in millimeters in carotid artery diameter between systole and diastole.
measure: Endothelial function evaluated by Endo-PAT2000® system
time frame: 12 months
description: Parameter measured as the reactive hyperemia index as calculated by the Endo-PAT2000® system software.
measure: Aortic valve calcification obtained from echocardiography.
time frame: 12 months
description: Parameter measured using a semi-quantitative scoring system based on scale of 1-4 as described by Rosenhek et al, New England Journal of Medicine 2000;343 (9):611.
1-no calcification, 2-mildly calcified (small isolated spots), 3-moderately calcified (multiple larger spots), 4-heavily calcified (extensive thickening and calcification of all cusps).
measure: Calcification of the aorta obtained by plain lateral radiography.
time frame: 12 months
description: Parameter measured using a semi-quantitative scoring system based on a scale of 0-3 as described by Kauppila et al, Atherosclerosis 1997;132:245.
0-no calcification, 1-small scattered calcific deposits filling less than 1/3 of the longitudinal wall of the aorta, 2-one third or more, but less than two thirds of the longitudinal wall of the aorta calcified, 3-two thirds or more of the longitudinal wall of the aorta calcified.
measure: Bone mineral density
time frame: 12 months
description: Osteodensitometry of the lumbar spine, hip, and distal radius, using dual-energy X-ray absorptiometry and reported in grams per square centimeter.
measure: Parathyroid hormone levels
time frame: 12 months
description: Measurement of parathyroid hormone levels using a commercially available intact parathyroid hormone ELISA kit with values reported in ng/L.
arm group label: Vitamin D3 5,000 units per week
arm group type: Active Comparator
description: Patient receive a dose that is considered within the standard dosing range for Vitamin D3 for one year.
arm group label: Vitamin D3 50,000 units per week
arm group type: Experimental
description: Patients receive a more aggressive Vitamin D3 dosing regimen of 50,000 units weekly for the first 3 months. At this point Vitamin D3 levels are measured. If the patient is Vitamin D3 replete (>75 nmol/L) then the dose is reduced to the equivalent of 25,000 units per week for the next 9 months. If the level is below this threshold then 50,000 units per week is continued for the next 9 months
intervention type: Drug
intervention name: Vitamin D3
description: Two different doses of Vitamin D3
arm group label: Vitamin D3 5,000 units per week
arm group label: Vitamin D3 50,000 units per week
other name: cholecalciferol
criteria: 
gender: All
minimum age: 18 Years
maximum age: 75 Years
healthy volunteers: No
last name: Mark L Lipman, M.D.
role: Principal Investigator
affiliation: Jewish General Hospital
facility: 
country: Canada
citation: Guerin AP, Blacher J, Pannier B, Marchais SJ, Safar ME, London GM. Impact of aortic stiffness attenuation on survival of patients in end-stage renal failure. Circulation. 2001 Feb 20;103(7):987-92. doi: 10.1161/01.cir.103.7.987.
PMID: 11181474
citation: London GM, Guerin AP, Verbeke FH, Pannier B, Boutouyrie P, Marchais SJ, Metivier F. Mineral metabolism and arterial functions in end-stage renal disease: potential role of 25-hydroxyvitamin D deficiency. J Am Soc Nephrol. 2007 Feb;18(2):613-20. doi: 10.1681/ASN.2006060573. Epub 2007 Jan 3.
PMID: 17202417
citation: Kendrick J, Targher G, Smits G, Chonchol M. 25-Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. Atherosclerosis. 2009 Jul;205(1):255-60. doi: 10.1016/j.atherosclerosis.2008.10.033. Epub 2008 Nov 11.
PMID: 19091317
citation: Motiwala SR, Wang TJ. Vitamin D and cardiovascular disease. Curr Opin Nephrol Hypertens. 2011 Jul;20(4):345-53. doi: 10.1097/MNH.0b013e3283474985.
PMID: 21519252
citation: Artaza JN, Mehrotra R, Norris KC. Vitamin D and the cardiovascular system. Clin J Am Soc Nephrol. 2009 Sep;4(9):1515-22. doi: 10.2215/CJN.02260409. Epub 2009 Aug 20.
PMID: 19696220
citation: Barreto DV, Barreto FC, Liabeuf S, Temmar M, Boitte F, Choukroun G, Fournier A, Massy ZA. Vitamin D affects survival independently of vascular calcification in chronic kidney disease. Clin J Am Soc Nephrol. 2009 Jun;4(6):1128-35. doi: 10.2215/CJN.00260109. Epub 2009 May 14.
PMID: 19443628
responsible party type: Principal Investigator
investigator affiliation: Jewish General Hospital
investigator full name: Mark L. Lipman
investigator title: Associate Professor of Medicine
mesh term: Bone Diseases
mesh term: Bone Diseases, Metabolic
mesh term: Kidney Diseases
mesh term: Renal Insufficiency, Chronic
mesh term: Renal Insufficiency
mesh term: Metabolic Diseases
mesh term: Vitamin D
mesh term: Cholecalciferol
sharing ipd: No