title: Podocyte as a potential target of inflammation: role of pioglitazone hydrochloride in patients with type 2 diabetes.
abstract: OBJECTIVE
  To observe the effects of pioglitazone hydrochloride on urinary sediment podocalyxin and monocyte chemoattractant protein-1 (MCP-1) excretion in patients with type 2 diabetes and to explore its possible renoprotective mechanisms.
  
  
  METHODS
  Ninety-eight patients with uncontrolled type 2 diabetes, who were previously prescribed metformin, acarbose, or both, were randomly assigned to a DP group (add-on pioglitazone; n = 49) or a DS group (add-on sulfonylurea; n = 49).
  
  
  RESULTS
  After 12 weeks of treatment, both add-on pioglitazone therapy (the DP group) and add-on sulfonylurea therapy (the DS group) demonstrated a similar improvement in fasting blood glucose and hemoglobin A1c, but systolic and diastolic blood pressure declined significantly in only the DP group. Moreover, the DP group showed significantly better efficacy in reducing urinary MCP-1 excretion in comparison with the DS group. Furthermore, both urinary albumin and urinary sediment podocalyxin excretion decreased significantly in the DP group but not in the DS group. The urinary sediment podocalyxin to creatinine ratio had a positive correlation with urinary albumin to creatinine ratio (r = 0.624; P<.01) and urinary MCP-1 to creatinine ratio (r = 0.346; P<.01).
  
  
  CONCLUSIONS
  Pioglitazone treatment revealed a podocyte-protective capacity in patients with type 2 diabetes, and the underlying mechanisms may be partly attributed to its effective suppression of excessive local renal inflammation.
authors.affiliation: Department of Endocrinology, Anhui Provincial Hospital, Hefei, Anhui, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Xing
authors.forename: Shandong
authors.initials: S
authors.lastname: Ye
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Hu
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
mesh_terms: D020909:Acarbose / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000652:urine; D018932:Chemokine CCL2 / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000276:immunology / Q000652:urine; D003928:Diabetic Nephropathies / Q000276:immunology / Q000517:prevention & control*; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control*; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008297:Male; D008687:Metformin / Q000627:therapeutic use; D008875:Middle Aged; D000077205:Pioglitazone; D050199:Podocytes / Q000187:drug effects* / Q000276:immunology; D020011:Protective Agents / Q000627:therapeutic use; D012795:Sialoglycoproteins / Q000737:chemistry / Q000652:urine; D012995:Solubility; D045162:Thiazolidinediones / Q000627:therapeutic use*
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D007004:Hypoglycemic Agents; D020011:Protective Agents; D012795:Sialoglycoproteins; D045162:Thiazolidinediones; C001643:podocalyxin; D008687:Metformin; D020909:Acarbose; D000077205:Pioglitazone