<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/NCT01680198</url>
  </required_header>
  <id_info>
    <org_study_id>Oct2010PENNYStudy</org_study_id>
    <nct_id>NCT01680198</nct_id>
  </id_info>
  <brief_title>Paricalcitol and Endothelial Function in Chronic Kidney Disease Patients (the PENNY Study)</brief_title>
  <acronym>PENNY</acronym>
  <official_title>Effect of Paricalcitol on Endothelial Function in Chronic Kidney Disease (CKD) Patients (the PENNY Study)</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Fondazione C.N.R./Regione Toscana &quot;G. Monasterio&quot;, Pisa, Italy</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Fondazione C.N.R./Regione Toscana &quot;G. Monasterio&quot;, Pisa, Italy</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      The primary aim of this study was to test the hypothesis that Paricalcitol, an active form of&#xD;
      vitamin D, improved endothelial function in stage 3-4 chronic kidney disease (CKD) patients.&#xD;
      A secondary aim of this trial was to study the relationship between endothelial function and&#xD;
      plasma/serum and genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin&#xD;
      angiotensin-aldosteron system (RAS) (angiotensin II and plasma renin activity).&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Primary objective: Test the hypothesis that Paricalcitol, an active form of vitamin D&#xD;
      improves endothelial function in stage 3-4 chronic kidney disease (CKD) patients.&#xD;
&#xD;
      Secondary analysis: Study the relationship between endothelial function and plasma/serum and&#xD;
      genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin&#xD;
      angiotensin-aldosteron system (RAS) (angiotensin II and plasma renin activity).&#xD;
&#xD;
      Background:&#xD;
&#xD;
      Endothelial function is altered in patients with CKD. Factors responsible for disturbed&#xD;
      endothelium-dependent vasodilatation in CKD include reduced bioactivity of the nitric oxide&#xD;
      (NO) pathway with decreased endothelial NO synthase (NOS) activity or inhibition via&#xD;
      accumulation of endogenous inhibitors. In patients with CKD and in those on dialysis serum&#xD;
      25(OH)D3 and 1,25(OH)2D3 levels are associated with FMD. Vitamin D receptors and 1&#xD;
      -hydroxylase activity are present in endothelial and vascular smooth muscle cells and&#xD;
      1,25(OH)2D3 stimulates vascular endothelial growth factor and prostacyclin production by&#xD;
      vascular smooth muscle cells. These biological observations may have clinical implications&#xD;
      because paricalcitol treatment predicts longer survival in ESRD patients and very recent data&#xD;
      link vitamin D to progression to ESRD in patients with stage 3-5 CKD. Furthermore, a previous&#xD;
      study by us has shown that the BMSI polymorphism of the vitamin D receptor gene is associated&#xD;
      with LVH and LVH progression in ESRD patients.&#xD;
&#xD;
      Study population: Patients with stage 3-4 CKD of both sexes in the age range 18-80 years.&#xD;
      Patients taking vitamin D supplements, with abnormal liver function tests, symptomatic&#xD;
      cardiovascular disease, diabetes or cancer and those whose medications changed during the&#xD;
      study were excluded.&#xD;
&#xD;
      Design and Methods: The study was a double-blind, randomized, parallel groups trial. After&#xD;
      baseline measurements, patients with iPTH level &gt; 65 pg/ml; Ca between 8.4- 10.00 mg/dL and P&#xD;
      between 2.9-4.5 were randomized to receive 2 micrograms Paricalcitol capsules (or matching&#xD;
      placebo) daily, for 12 weeks. This doses was adjusted based on clinical laboratory parameters&#xD;
      and the maximum dose was 2 micrograms daily.&#xD;
&#xD;
      During the study if a subject experienced over suppression of serum iPTH (defined as a serum&#xD;
      iPTH &lt;15 pg/mL), or hypercalcemia (defined as Ca &gt; 11.0 mg/dL), the subject continued to take&#xD;
      study drug at reduced dosage 1 mcg any other day and returned in 2 weeks for an unscheduled&#xD;
      visit. If the values from the unscheduled visit serum iPTH and/or Ca did not returned to &gt; 15&#xD;
      pg/mL and/or &lt;11.0 mg/dL, respectively, the drug was discontinued.&#xD;
&#xD;
      Flow mediated vasodilatation was measured according to a validated protocol developed at the&#xD;
      coordinating center of a national (Italian)working group of vascular function testing.&#xD;
&#xD;
      Primary end-point: Change in Flow Mediated Dilatation (FMD) induced by Paricalcitol in&#xD;
      comparison to Placebo.&#xD;
&#xD;
      Study power: To detect a 2% difference (standard deviation: ± 3.0%) in the change in FMD&#xD;
      between Paracalcitol treated and untreated patients with a power of 80 %, a confidence level&#xD;
      using a two-tailed test of 5% and a potential attrition rate of 15%, at least 44 patients per&#xD;
      group were required (88 patients in total).&#xD;
&#xD;
      Statistical analysis: Data will be summarized as mean ± standard deviation (normally&#xD;
      distributed data), median and inter-quartile range (non normally distributed data) or as&#xD;
      percent frequency, and comparison between groups will be made by independent T-Test,&#xD;
      Mann-Whitney Test, or Chi Square test, as appropriate. Within patients comparisons will be&#xD;
      done by statistical tests for paired observations. Data analysis of the primary outcome will&#xD;
      be performed by comparing the changes in FMD in Paracalcitol treated and untreated patients&#xD;
      by using the T-Test for independent observations. Possible differences in risk factors at&#xD;
      baseline not controlled by randomization (i.e. differences due to chance) will be accounted&#xD;
      for by using multivariate regression analyses.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date>June 2011</start_date>
  <completion_date type="Actual">August 2012</completion_date>
  <primary_completion_date type="Actual">August 2012</primary_completion_date>
  <phase>Phase 3</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>Triple (Participant, Investigator, Outcomes Assessor)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>Endothelial function measurement</measure>
    <time_frame>12 weeks from baseline</time_frame>
    <description>Endothelial-dependent and independent vasodilation was assessed by a Toshiba Nemia XG Echo-Doppler applying a 7.5 MHz transducer that was fixed by an adjustable stereotactic clamp to warrant image stability. After baseline recording (1 min) a standard sphygmomanometer was placed on the right forearm 2 cm below the elbow and the cuff was inflated to 250 mmHg for 5 min. Recordings were performed during the 4 min following cuff deflation to estimate endothelium-dependent FMD. In studies of endothelium-independent vasodilatation recording times were 1 min for the baseline assessment and 5 min for changes in arterial diameter brought about by GTN. An interval of at least 1h was set between the last FMD assessment and GTN administration. All scans were recorded, stored and analyzed off-line. FMD and GTN were computed as the maximal % increase in diameter over baseline by an automatic edge detection system.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Endothelial function and plasma/serum and genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin angiotensin-aldosteron system (RAS).</measure>
    <time_frame>12 weeks from baseline</time_frame>
    <description>The investigators will analyze the relationship between endothelial function and plasma/serum and genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin angiotensin-aldosteron system (RAS) (angiotensin II and plasma renin activity).</description>
  </secondary_outcome>
  <number_of_arms>2</number_of_arms>
  <enrollment type="Actual">88</enrollment>
  <condition>Chronic Kidney Disease.</condition>
  <arm_group>
    <arm_group_label>Placebo</arm_group_label>
    <arm_group_type>Placebo Comparator</arm_group_type>
    <description>Placebo capsules daily for 12 weeks.</description>
  </arm_group>
  <arm_group>
    <arm_group_label>Paracalcitol</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>see &quot;Intervention description&quot; for details.</description>
  </arm_group>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Paracalcitol</intervention_name>
    <description>Patients in the experimental arm received 2 micrograms Paricalcitol capsules daily, for 12 weeks. This dose was adjusted based on clinical laboratory parameters and the maximum dose was 2 micrograms daily.</description>
    <arm_group_label>Paracalcitol</arm_group_label>
    <other_name>Active form of Vitamin D.</other_name>
  </intervention>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>placebo</intervention_name>
    <arm_group_label>Placebo</arm_group_label>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Patients with iPTH level &gt; 65 pg/ml; Ca between 8.4- 10.00 mg/dL and P between 2.9-4.5&#xD;
&#xD;
          -  Negative serum pregnancy test for female subjects of childbering potential.&#xD;
&#xD;
          -  Informed consent.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  Use vitamin D supplements.&#xD;
&#xD;
          -  Altered liver function tests (bilirubin, aminotransferases and total alkaline&#xD;
             phosphatase &gt; 3 times the upper limit of normal ranges).&#xD;
&#xD;
          -  Sympthomatic cardiovascular disease on the basis of clinical history. Cancer.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>80 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Giuseppe Curatola, MD</last_name>
    <role>Study Director</role>
    <affiliation>Nephrology, Dialysis and Transplantation Unit</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>Nephrology, Dialysis and Transplantation Unit</name>
      <address>
        <city>Reggio Calabria</city>
        <zip>89124</zip>
        <country>Italy</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Italy</country>
  </location_countries>
  <reference>
    <citation>Yilmaz MI, Sonmez A, Saglam M, Yaman H, Kilic S, Demirkaya E, Eyileten T, Caglar K, Oguz Y, Vural A, Yenicesu M, Zoccali C. FGF-23 and vascular dysfunction in patients with stage 3 and 4 chronic kidney disease. Kidney Int. 2010 Oct;78(7):679-85. doi: 10.1038/ki.2010.194. Epub 2010 Jul 7.</citation>
    <PMID>20613714</PMID>
  </reference>
  <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>
  </reference>
  <reference>
    <citation>Yamamoto T, Kozawa O, Tanabe K, Akamatsu S, Matsuno H, Dohi S, Hirose H, Uematsu T. 1,25-dihydroxyvitamin D3 stimulates vascular endothelial growth factor release in aortic smooth muscle cells: role of p38 mitogen-activated protein kinase. Arch Biochem Biophys. 2002 Feb 1;398(1):1-6. doi: 10.1006/abbi.2001.2632.</citation>
    <PMID>11811942</PMID>
  </reference>
  <reference>
    <citation>Wakasugi M, Noguchi T, Inoue M, Kazama Y, Tawata M, Kanemaru Y, Onaya T. Vitamin D3 stimulates the production of prostacyclin by vascular smooth muscle cells. Prostaglandins. 1991 Aug;42(2):127-36. doi: 10.1016/0090-6980(91)90072-n.</citation>
    <PMID>1775635</PMID>
  </reference>
  <reference>
    <citation>Teng M, Wolf M, Ofsthun MN, Lazarus JM, Hernan MA, Camargo CA Jr, Thadhani R. Activated injectable vitamin D and hemodialysis survival: a historical cohort study. J Am Soc Nephrol. 2005 Apr;16(4):1115-25. doi: 10.1681/ASN.2004070573. Epub 2005 Feb 23.</citation>
    <PMID>15728786</PMID>
  </reference>
  <reference>
    <citation>Teng M, Wolf M, Lowrie E, Ofsthun N, Lazarus JM, Thadhani R. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med. 2003 Jul 31;349(5):446-56. doi: 10.1056/NEJMoa022536.</citation>
    <PMID>12890843</PMID>
  </reference>
  <reference>
    <citation>Ravani P, Malberti F, Tripepi G, Pecchini P, Cutrupi S, Pizzini P, Mallamaci F, Zoccali C. Vitamin D levels and patient outcome in chronic kidney disease. Kidney Int. 2009 Jan;75(1):88-95. doi: 10.1038/ki.2008.501. Epub 2008 Oct 8.</citation>
    <PMID>18843258</PMID>
  </reference>
  <reference>
    <citation>Testa A, Mallamaci F, Benedetto FA, Pisano A, Tripepi G, Malatino L, Thadhani R, Zoccali C. Vitamin D receptor (VDR) gene polymorphism is associated with left ventricular (LV) mass and predicts left ventricular hypertrophy (LVH) progression in end-stage renal disease (ESRD) patients. J Bone Miner Res. 2010 Feb;25(2):313-9. doi: 10.1359/jbmr.090717.</citation>
    <PMID>20422622</PMID>
  </reference>
  <reference>
    <citation>Ghiadoni L, Faita F, Salvetti M, Cordiano C, Biggi A, Puato M, Di Monaco A, De Siati L, Volpe M, Ambrosio G, Gemignani V, Muiesan ML, Taddei S, Lanza GA, Cosentino F. Assessment of flow-mediated dilation reproducibility: a nationwide multicenter study. J Hypertens. 2012 Jul;30(7):1399-405. doi: 10.1097/HJH.0b013e328353f222.</citation>
    <PMID>22525207</PMID>
  </reference>
  <verification_date>October 2012</verification_date>
  <study_first_submitted>August 30, 2012</study_first_submitted>
  <study_first_submitted_qc>September 6, 2012</study_first_submitted_qc>
  <study_first_posted type="Estimate">September 7, 2012</study_first_posted>
  <last_update_submitted>October 1, 2012</last_update_submitted>
  <last_update_submitted_qc>October 1, 2012</last_update_submitted_qc>
  <last_update_posted type="Estimate">October 2, 2012</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>Fondazione C.N.R./Regione Toscana &quot;G. Monasterio&quot;, Pisa, Italy</investigator_affiliation>
    <investigator_full_name>Carmine Zoccali</investigator_full_name>
    <investigator_title>Prof.</investigator_title>
  </responsible_party>
  <keyword>Vitamin D</keyword>
  <keyword>Paracalcitol</keyword>
  <keyword>Chronic kidney disease</keyword>
  <keyword>Endothelial dysfunction</keyword>
  <keyword>Flow mediated vasodilation</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Kidney Diseases</mesh_term>
    <mesh_term>Renal Insufficiency, Chronic</mesh_term>
  </condition_browse>
  <intervention_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Vitamin D</mesh_term>
  </intervention_browse>
  <!-- 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/NCT01680198
org study id: Oct2010PENNYStudy
nct id: NCT01680198
lead sponsor: 
has dmc: Yes
The primary aim of this study was to test the hypothesis that Paricalcitol, an active form of
      vitamin D, improved endothelial function in stage 3-4 chronic kidney disease (CKD) patients.
      A secondary aim of this trial was to study the relationship between endothelial function and
      plasma/serum and genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin
      angiotensin-aldosteron system (RAS) (angiotensin II and plasma renin activity).
Primary objective: Test the hypothesis that Paricalcitol, an active form of vitamin D
      improves endothelial function in stage 3-4 chronic kidney disease (CKD) patients.

      Secondary analysis: Study the relationship between endothelial function and plasma/serum and
      genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin
      angiotensin-aldosteron system (RAS) (angiotensin II and plasma renin activity).

      Background:

      Endothelial function is altered in patients with CKD. Factors responsible for disturbed
      endothelium-dependent vasodilatation in CKD include reduced bioactivity of the nitric oxide
      (NO) pathway with decreased endothelial NO synthase (NOS) activity or inhibition via
      accumulation of endogenous inhibitors. In patients with CKD and in those on dialysis serum
      25(OH)D3 and 1,25(OH)2D3 levels are associated with FMD. Vitamin D receptors and 1
      -hydroxylase activity are present in endothelial and vascular smooth muscle cells and
      1,25(OH)2D3 stimulates vascular endothelial growth factor and prostacyclin production by
      vascular smooth muscle cells. These biological observations may have clinical implications
      because paricalcitol treatment predicts longer survival in ESRD patients and very recent data
      link vitamin D to progression to ESRD in patients with stage 3-5 CKD. Furthermore, a previous
      study by us has shown that the BMSI polymorphism of the vitamin D receptor gene is associated
      with LVH and LVH progression in ESRD patients.

      Study population: Patients with stage 3-4 CKD of both sexes in the age range 18-80 years.
      Patients taking vitamin D supplements, with abnormal liver function tests, symptomatic
      cardiovascular disease, diabetes or cancer and those whose medications changed during the
      study were excluded.

      Design and Methods: The study was a double-blind, randomized, parallel groups trial. After
      baseline measurements, patients with iPTH level > 65 pg/ml; Ca between 8.4- 10.00 mg/dL and P
      between 2.9-4.5 were randomized to receive 2 micrograms Paricalcitol capsules (or matching
      placebo) daily, for 12 weeks. This doses was adjusted based on clinical laboratory parameters
      and the maximum dose was 2 micrograms daily.

      During the study if a subject experienced over suppression of serum iPTH (defined as a serum
      iPTH <15 pg/mL), or hypercalcemia (defined as Ca > 11.0 mg/dL), the subject continued to take
      study drug at reduced dosage 1 mcg any other day and returned in 2 weeks for an unscheduled
      visit. If the values from the unscheduled visit serum iPTH and/or Ca did not returned to > 15
      pg/mL and/or <11.0 mg/dL, respectively, the drug was discontinued.

      Flow mediated vasodilatation was measured according to a validated protocol developed at the
      coordinating center of a national (Italian)working group of vascular function testing.

      Primary end-point: Change in Flow Mediated Dilatation (FMD) induced by Paricalcitol in
      comparison to Placebo.

      Study power: To detect a 2% difference (standard deviation: ± 3.0%) in the change in FMD
      between Paracalcitol treated and untreated patients with a power of 80 %, a confidence level
      using a two-tailed test of 5% and a potential attrition rate of 15%, at least 44 patients per
      group were required (88 patients in total).

      Statistical analysis: Data will be summarized as mean ± standard deviation (normally
      distributed data), median and inter-quartile range (non normally distributed data) or as
      percent frequency, and comparison between groups will be made by independent T-Test,
      Mann-Whitney Test, or Chi Square test, as appropriate. Within patients comparisons will be
      done by statistical tests for paired observations. Data analysis of the primary outcome will
      be performed by comparing the changes in FMD in Paracalcitol treated and untreated patients
      by using the T-Test for independent observations. Possible differences in risk factors at
      baseline not controlled by randomization (i.e. differences due to chance) will be accounted
      for by using multivariate regression analyses.
allocation: Randomized
intervention model: Parallel Assignment
primary purpose: Treatment
masking: Triple (Participant, Investigator, Outcomes Assessor)
measure: Endothelial function measurement
time frame: 12 weeks from baseline
description: Endothelial-dependent and independent vasodilation was assessed by a Toshiba Nemia XG Echo-Doppler applying a 7.5 MHz transducer that was fixed by an adjustable stereotactic clamp to warrant image stability. After baseline recording (1 min) a standard sphygmomanometer was placed on the right forearm 2 cm below the elbow and the cuff was inflated to 250 mmHg for 5 min. Recordings were performed during the 4 min following cuff deflation to estimate endothelium-dependent FMD. In studies of endothelium-independent vasodilatation recording times were 1 min for the baseline assessment and 5 min for changes in arterial diameter brought about by GTN. An interval of at least 1h was set between the last FMD assessment and GTN administration. All scans were recorded, stored and analyzed off-line. FMD and GTN were computed as the maximal % increase in diameter over baseline by an automatic edge detection system.
measure: Endothelial function and plasma/serum and genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin angiotensin-aldosteron system (RAS).
time frame: 12 weeks from baseline
description: The investigators will analyze the relationship between endothelial function and plasma/serum and genetic biomarkers of bone mineral disorders in CKD (BMD-CKD) and renin angiotensin-aldosteron system (RAS) (angiotensin II and plasma renin activity).
arm group label: Placebo
arm group type: Placebo Comparator
description: Placebo capsules daily for 12 weeks.
arm group label: Paracalcitol
arm group type: Experimental
description: see "Intervention description" for details.
intervention type: Drug
intervention name: Paracalcitol
description: Patients in the experimental arm received 2 micrograms Paricalcitol capsules daily, for 12 weeks. This dose was adjusted based on clinical laboratory parameters and the maximum dose was 2 micrograms daily.
arm group label: Paracalcitol
other name: Active form of Vitamin D.
intervention type: Drug
intervention name: placebo
arm group label: Placebo
criteria: 
gender: All
minimum age: 18 Years
maximum age: 80 Years
healthy volunteers: No
last name: Giuseppe Curatola, MD
role: Study Director
affiliation: Nephrology, Dialysis and Transplantation Unit
facility: 
country: Italy
citation: Yilmaz MI, Sonmez A, Saglam M, Yaman H, Kilic S, Demirkaya E, Eyileten T, Caglar K, Oguz Y, Vural A, Yenicesu M, Zoccali C. FGF-23 and vascular dysfunction in patients with stage 3 and 4 chronic kidney disease. Kidney Int. 2010 Oct;78(7):679-85. doi: 10.1038/ki.2010.194. Epub 2010 Jul 7.
PMID: 20613714
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: Yamamoto T, Kozawa O, Tanabe K, Akamatsu S, Matsuno H, Dohi S, Hirose H, Uematsu T. 1,25-dihydroxyvitamin D3 stimulates vascular endothelial growth factor release in aortic smooth muscle cells: role of p38 mitogen-activated protein kinase. Arch Biochem Biophys. 2002 Feb 1;398(1):1-6. doi: 10.1006/abbi.2001.2632.
PMID: 11811942
citation: Wakasugi M, Noguchi T, Inoue M, Kazama Y, Tawata M, Kanemaru Y, Onaya T. Vitamin D3 stimulates the production of prostacyclin by vascular smooth muscle cells. Prostaglandins. 1991 Aug;42(2):127-36. doi: 10.1016/0090-6980(91)90072-n.
PMID: 1775635
citation: Teng M, Wolf M, Ofsthun MN, Lazarus JM, Hernan MA, Camargo CA Jr, Thadhani R. Activated injectable vitamin D and hemodialysis survival: a historical cohort study. J Am Soc Nephrol. 2005 Apr;16(4):1115-25. doi: 10.1681/ASN.2004070573. Epub 2005 Feb 23.
PMID: 15728786
citation: Teng M, Wolf M, Lowrie E, Ofsthun N, Lazarus JM, Thadhani R. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med. 2003 Jul 31;349(5):446-56. doi: 10.1056/NEJMoa022536.
PMID: 12890843
citation: Ravani P, Malberti F, Tripepi G, Pecchini P, Cutrupi S, Pizzini P, Mallamaci F, Zoccali C. Vitamin D levels and patient outcome in chronic kidney disease. Kidney Int. 2009 Jan;75(1):88-95. doi: 10.1038/ki.2008.501. Epub 2008 Oct 8.
PMID: 18843258
citation: Testa A, Mallamaci F, Benedetto FA, Pisano A, Tripepi G, Malatino L, Thadhani R, Zoccali C. Vitamin D receptor (VDR) gene polymorphism is associated with left ventricular (LV) mass and predicts left ventricular hypertrophy (LVH) progression in end-stage renal disease (ESRD) patients. J Bone Miner Res. 2010 Feb;25(2):313-9. doi: 10.1359/jbmr.090717.
PMID: 20422622
citation: Ghiadoni L, Faita F, Salvetti M, Cordiano C, Biggi A, Puato M, Di Monaco A, De Siati L, Volpe M, Ambrosio G, Gemignani V, Muiesan ML, Taddei S, Lanza GA, Cosentino F. Assessment of flow-mediated dilation reproducibility: a nationwide multicenter study. J Hypertens. 2012 Jul;30(7):1399-405. doi: 10.1097/HJH.0b013e328353f222.
PMID: 22525207
responsible party type: Principal Investigator
investigator affiliation: Fondazione C.N.R./Regione Toscana "G. Monasterio", Pisa, Italy
investigator full name: Carmine Zoccali
investigator title: Prof.
mesh term: Kidney Diseases
mesh term: Renal Insufficiency, Chronic
mesh term: Vitamin D