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Prevention of Renal Complications of Diabetes With Thiamine

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ClinicalTrials.gov Identifier: NCT01725412
Recruitment Status : Unknown
Verified November 2012 by Gudrun Caspar-Bell, University of Saskatchewan.
Recruitment status was:  Not yet recruiting
First Posted : November 12, 2012
Last Update Posted : November 12, 2012
Information provided by (Responsible Party):
Gudrun Caspar-Bell, University of Saskatchewan

Brief Summary:
Thiamine is a key component in the creation of physiologic anti-inflammatory mediators. Serum thiamine stores have been found to be deficient in diabetic patients. Thiamine deficiency may be a key pathological mechanism of inflammation that results in diabetic kidney and retinal injury. The investigators hypothesize that the repletion of a patient's thiamine by oral supplementation may result in reduced inflammation, and therefore reduced kidney injury.

Condition or disease Intervention/treatment Phase
Diabetic Nephropathy Dietary Supplement: Thiamine 300mg PO once daily Dietary Supplement: placebo Phase 4

Detailed Description:

Thiamine (vitamin B1) is a water-soluble vitamin. It is absorbed from the gastrointestinal tract and taken up into tissues by transport proteins and converted to thiamine pyrophosphate (TPP) by thiamine pyrophosphokinase (TPPK). TPP is a co-factor of pyruvate dehydrogenase (PDH), α-ketoglutarate dehydrogenase and transketolase (TKT)—enzymes involved in the metabolism of glucose.

Various transport proteins are involved in the transport of thiamine monophosphate (TMP) and TPP across membranes. These include thiamine transported isoform-1 (THTR1) and thiamine transporter isoform-2 (THTR2), reduced folate carrier-1 (RFC-1), which transports TMP and TPP across cell plasma membranes and the mitochondrial TPP transporter (mTHTR). Thiamine and TMP/TPP transporters may have abnormal expression in diabetes. Increased THTR1 levels are found in red blood cells (RBCs) and mononuclear leucocytes of patients with diabetes compared to those of healthy subjects. RBC precursors and leucocytes appeared to up-regulate THTR1 expression in response to decreased thiamine availability. In the presence of hyperglycemia, renal tubular epithelial cells, by contrast, have decreased expression. In both experimental models of diabetes and in human diabetics increased clearance of thiamine has been demonstrated. This precedes the development of microalbuminuria. Patients with microalbuminuria and early decline in glomerular filtration rate had higher fractional excretion of thiamine compared to patients with stable renal function.

Thiamine supplementation in STZ- diabetic mice prevented the development of microalbuminuria, decreasing urinary albumin excretion (UAE) by approximately 80%. In addition thiamine supplementation prevented diuresis and glycosuria. Human studies are limited but in one placebo controlled study the thiamine group showed a significant decrease in microalbuminuria in diabetic patients on thiamine.

Study Type : Interventional  (Clinical Trial)
Estimated Enrollment : 40 participants
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Triple (Participant, Care Provider, Investigator)
Primary Purpose: Treatment
Study Start Date : November 2012
Estimated Primary Completion Date : June 2013

Resource links provided by the National Library of Medicine

U.S. FDA Resources

Arm Intervention/treatment
Experimental: Thiamine Supplementation Dietary Supplement: Thiamine 300mg PO once daily
Placebo Comparator: Placebo Dietary Supplement: placebo

Primary Outcome Measures :
  1. Microabluminuria

Secondary Outcome Measures :
  1. Serum Thiamine Level

Other Outcome Measures:
  1. Urinary Thiamine Level
  2. Inflammatory Markers
    E-selectin, Intercellular Adhesion Molecule 1, von Willebrand Factor, malondialdehyde, glutathione, homocysteine, isoprotein F21, advanced glycation endproducts, receptor for advanced glycation endproducts

Information from the National Library of Medicine

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Ages Eligible for Study:   30 Years to 50 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No

Inclusion Criteria:

  • with a diagnosis of Type II diabetes which has been present for at least 5 years,
  • persistent microalbuminuria (30-299 mg/24 h),
  • HbA1c ≤ 8%, and
  • BMI 19-40 kg/m2.

Exclusion Criteria:

  • significant comorbidities,
  • "deficient renal function" known allergy or intolerance to thiamine,
  • use of thiamine supplements,
  • participation in an interventional study within 30 days,
  • recipients of renal and/or pancreatic transplant and
  • women who were pregnant or breast feeding.

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01725412

Contact: Gudrun Caspar-Bell, MD 306 966-2044 Gudrun.casparbell@saskatoonhealthregion.ca
Contact: Benjamin M Sehmer, MB 306 261 3932 benjamin.sehmer@usask.ca

Canada, Saskatchewan
Royal University Hospital Recruiting
Saskatoon, Saskatchewan, Canada, S7K 0M7
Contact: Gudrun Caspar-Bell         
Sponsors and Collaborators
University of Saskatchewan
Principal Investigator: Dr. Gudrun Caspar-Bell, MD University of Saskatchewan

Responsible Party: Gudrun Caspar-Bell, Endocrinologist, University of Saskatchewan
ClinicalTrials.gov Identifier: NCT01725412     History of Changes
Other Study ID Numbers: Bio REB #12-59
First Posted: November 12, 2012    Key Record Dates
Last Update Posted: November 12, 2012
Last Verified: November 2012

Additional relevant MeSH terms:
Diabetic Nephropathies
Kidney Diseases
Urologic Diseases
Diabetes Complications
Diabetes Mellitus
Endocrine System Diseases
Vitamin B Complex
Growth Substances
Physiological Effects of Drugs