title: Urinary PGDS levels are associated with vascular injury in type 2 diabetes patients.
abstract: BACKGROUND
  The presence of metabolic syndrome has been shown to be predictors of cardiovascular morbidity and mortality in patients with type 2 diabetes. In a cross-sectional clinical study, we investigated the association of metabolic syndrome with asymptomatic lacunar strokes and cardiovascular disease (CVD) and we compared its significance with urinary protein markers.
  
  
  METHODS
  We studied Japanese type 2 diabetes patients (n=233, men=124, women=109). The diagnosis of metabolic syndrome was made according to WHO and International Diabetes Federation (IDF) criteria. Cardiovascular events were recorded and asymptomatic lacunar lesions were evaluated with magnetic resonance imaging (MRI). We also measured urinary levels of albumin, type IV collagen, beta2-microglobulin (beta2MG), N-acetyl-beta-d-glucosaminidase (NAG) and lipocalin-type prostaglandin D synthase (PGDS).
  
  
  RESULTS
  The prevalence of metabolic syndrome is 31.3% (IDF) and 52% (WHO) in 233 patients and microalbuminuria was present in 62 subjects (26.6%). Metabolic syndrome (WHO) significantly associated with asymptomatic lacunar lesions (p=0.035, OR=2.854, CI 1.075-7.579), while metabolic syndrome (IDF) or urinary markers failed to associate with presence of asymptomatic lacunar lesions. The presence of metabolic syndrome or microalbuminuria did not show significant association with CVD; however, the elevation of beta2MG, NAG and PGDS showed significant association with CVD. By a logistic regression analysis using urinary proteins as independent variables, the presence of higher PGDS excretion independently associated with history of CVD (p=0.025, OR=3.847, CI 1.180-12.545).
  
  
  CONCLUSIONS
  In type 2 diabetes patients, the elevation of urinary PGDS secretion closely associated with cardiovascular events and may be a supplemental or additional marker to the criteria of metabolic syndrome.
authors.affiliation: Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Okayama, Japan.
authors.forename: Ritsuko
authors.initials: R
authors.lastname: Yoshikawa
authors.forename: Jun
authors.initials: J
authors.lastname: Wada
authors.forename: Kousuke
authors.initials: K
authors.lastname: Seiki
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsuoka
authors.forename: Satoshi
authors.initials: S
authors.lastname: Miyamoto
authors.forename: Kenji
authors.initials: K
authors.lastname: Takahashi
authors.forename: Sachiko
authors.initials: S
authors.lastname: Ota
authors.forename: Kazuhi
authors.initials: K
authors.lastname: Taniai
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Hida
authors.forename: Minoru
authors.initials: M
authors.lastname: Yamakado
authors.forename: Kenichi
authors.initials: K
authors.lastname: Shikata
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Uehara
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Urade
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Makino
mesh_terms: D000419:Albuminuria / Q000652:urine; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000473:pathology / Q000652:urine*; D002539:Cerebral Arterial Diseases / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000473:pathology / Q000652:urine*; D005260:Female; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000652:urine*; D054834:Lipocalins; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology* / Q000652:urine*; D008875:Middle Aged
chemical_list: D054834:Lipocalins; D019746:Intramolecular Oxidoreductases; C022466:prostaglandin R2 D-isomerase