title: Oral cholecalciferol decreases albuminuria and urinary TGF-β1 in patients with type 2 diabetic nephropathy on established renin-angiotensin-aldosterone system inhibition.
abstract: The anti-inflammatory, antifibrotic, and antiproteinuric properties of vitamin D have been defined in studies using active vitamin D analogs. In this prospective observational study we determined whether nutritional vitamin D repletion can have additional beneficial effects in patients with type 2 diabetic nephropathy already established on renin-angiotensin-aldosterone system inhibition. During a 7-month period, 63 patients were enrolled and those with low levels of 25(OH)D were treated with oral cholecalciferol for 4 months. Baseline serum 25(OH)D and 1,25(OH)(2)D showed no significant correlation with baseline urinary MCP-1, TGF-β1, or albuminuria measured as the urinary albumin-to-creatinine ratio. Of the 63 patients, 54 had insufficient or deficient levels of serum 25(OH)D and 49 complied with cholecalciferol therapy and follow-up. Both 25(OH)D and 1,25(OH)(2)D were significantly increased at 2 and 4 months of treatment. Albuminuria and urinary TGF-β1 decreased significantly at both time points compared to their baseline values, while urinary MCP-1 did not change. Thus, in the short term, dietary vitamin D repletion with cholecalciferol had a beneficial effect in delaying the progression of diabetic nephropathy above that due to established renin-angiotensin-aldosterone system inhibition.
authors.affiliation: Imperial College Kidney and Transplant Institute, Hammersmith Hospital, Imperial College London, London, UK. min-jeong.kim@imperial.ac.uk
authors.forename: Min Jeong
authors.initials: MJ
authors.lastname: Kim
authors.forename: Andrew H
authors.initials: AH
authors.lastname: Frankel
authors.forename: Mandy
authors.initials: M
authors.lastname: Donaldson
authors.forename: Sarah J
authors.initials: SJ
authors.lastname: Darch
authors.forename: Charles D
authors.initials: CD
authors.lastname: Pusey
authors.forename: Peter D
authors.initials: PD
authors.lastname: Hill
authors.forename: Michael
authors.initials: M
authors.lastname: Mayr
authors.forename: Frederick W K
authors.initials: FW
authors.lastname: Tam
mesh_terms: D000284:Administration, Oral; D000368:Aged; D000419:Albuminuria / Q000188:drug therapy* / Q000652:urine; D018932:Chemokine CCL2 / Q000652:urine; D002762:Cholecalciferol / Q000008:administration & dosage / Q000627:therapeutic use*; D003404:Creatinine / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003928:Diabetic Nephropathies / Q000188:drug therapy*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D053773:Transforming Growth Factor beta1 / Q000652:urine*; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood; D014809:Vitamin D-Binding Protein / Q000652:urine
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D053773:Transforming Growth Factor beta1; D014809:Vitamin D-Binding Protein; D014807:Vitamin D; D002762:Cholecalciferol; C104450:25-hydroxyvitamin D; D003404:Creatinine