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Salt Intake and Antiproteinuric Effect of Paricalcitol in Type 2 Diabetes (PROCEED)

This study is currently recruiting participants. (see Contacts and Locations)
Verified September 2014 by Mario Negri Institute for Pharmacological Research
Sponsor:
Collaborator:
Abbott
Information provided by (Responsible Party):
Mario Negri Institute for Pharmacological Research
ClinicalTrials.gov Identifier:
NCT01393808
First received: July 12, 2011
Last updated: September 17, 2014
Last verified: September 2014

July 12, 2011
September 17, 2014
September 2011
June 2015   (final data collection date for primary outcome measure)
Changes in urinary albumin excretion from baseline at 4 month. [ Time Frame: At baseline and 1,2,3 and 4 month. ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT01393808 on ClinicalTrials.gov Archive Site
  • Ambulatory and 24-hour blood pressure profile. [ Time Frame: At 1 month. ] [ Designated as safety issue: No ]
  • Ambulatory and 24-hour blood pressure profile. [ Time Frame: At 2 month. ] [ Designated as safety issue: No ]
  • Ambulatory and 24-hour blood pressure profile. [ Time Frame: At 3 month. ] [ Designated as safety issue: No ]
  • Ambulatory and 24-hour blood pressure profile. [ Time Frame: At 4 month. ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Salt Intake and Antiproteinuric Effect of Paricalcitol in Type 2 Diabetes
A Prospective, Randomized, Cross-over, Double-blind, Placebo-controlled Study to Assess the Antiproteinuric Effect of Selective Vitamin d Receptor Activation by Paricalcitol in Type 2 Diabetes Patients on Low or High Sodium Diet and Stable Ras Inhibitor Therapy

Proteinuria is an independent risk factor for cardiovascular morbidity and mortality and for renal disease progression. More proteinuria is associated with faster progression, whereas treatments that reduce proteinuria are renoprotective in both diabetic and non diabetic chronic kidney disease. Of note, lower the residual proteinuria achieved by treatment slower is the disease progression in the long term. On the basis of the above findings, proteinuria has become a target of renoprotective therapy.

Among different antihypertensive medications, those that inhibit the Renin Angiotensin System, such as angiotensin converting enzyme (ACE)inhibitors and angiotensin receptor blockers (ARBs), are those that at comparable blood pressure control, more effectively reduce proteinuria and slow renal disease progression. Thus they have become the key component of renoprotective therapy in patients with proteinuric chronic kidney disease. Observational studies found that their effectiveness, however, is limited or even fully blunted in patients who eat large amount of salt.

Experimental evidence indicates a renoprotective role of the vitamin D system in chronic renal disease. A recent randomized, controlled trial, add-on therapy with selective Vitamin D receptor activator paricalcitol showed an additive antiproteinuric effect in subjects with type 2 diabetes and chronic kidney disease on background Renin-angiotensin-system inhibitor therapy. This effect, however, was largely restricted to subjects with daily sodium intake exceeding 12 grams and was negligible in those with lower sodium intake. Thus, treatment with paricalcitol appears to be effective in particular in those patients who do not appreciably benefit of renin angiotensin system (RAS) inhibitors therapy because of high salt intake. Thus, whether the antiproteinuric effect of paricalcitol is modified by concomitant salt intake in patients with chronic kidney disease (CKD) on background RAS inhibitors therapy, is worth investigating.

The broad aim of this study is to evaluate the interaction between paricalcitol therapy and sodium intake in type 2 diabetes patients with proteinuric kidney disease on stable background RAS inhibitor therapy.

Not Provided
Interventional
Phase 2
Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
Type 2 Diabetes
  • Drug: Paricalcitol
    1-month Paricalcitol 2mcg/day
  • Other: placebo
    1-month Placebo Treatment
  • Experimental: Paricalcitol
    Intervention: Drug: Paricalcitol
  • Placebo Comparator: placebo
    Intervention: Other: placebo
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
112
December 2015
June 2015   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Male and female patients;
  • Age > 18 years;
  • Type 2 diabetes patients on low or high sodium diet and stable RAS inhibitor therapy with the following conditions:

Urinary albumin excretion (UAE) rate >300mg/24 hours (200 mcg/min); Serum creatinine <2 mg/dL, PTH ≥ 20 mEq/L and <110 mEq/L; Calcium and phosphorus levels < 9.5 mg/dl and < 5mg/dl, respectively; Controlled BP (systolic/diastolic <140/90 mmHg) while on stable RAS inhibitor therapy;

- Written informed consent.

Exclusion Criteria:

  • Previous Vitamin D or Vitamin D analogs therapy (within 3 months prior to the study entry);
  • Evidence of toxicity to Vitamin D;
  • History of kidney stones;
  • Poorly controlled Diabetes: Hb1Ac > 12%;
  • Therapy with calcitonin, bisphosphonates, cinacalcet, glucocorticoids, immunosuppressive drugs or other drug that may affect calcium or bone metabolism;
  • Cancer and any severe systemic disease or clinical condition that may jeopardize data interpretation or completion of the study;
  • Any clinically relevant conditions that might affect study participation and/or study results;
  • Any contraindication to be exposed to Paricalcitol;
  • Pregnancy or lactating;
  • Women of childbearing potential without following a scientifically accepted form of contraception;
  • Legal incapacity.
Both
18 Years to 80 Years
No
Contact: Piero Ruggenenti, MD 0039 035 45351 piero.ruggenenti@marionegri.it
Italy
 
NCT01393808
PROCEED, 2011-001713-14
No
Mario Negri Institute for Pharmacological Research
Mario Negri Institute for Pharmacological Research
Abbott
Not Provided
Mario Negri Institute for Pharmacological Research
September 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP