title: Lipocalin-type prostaglandin d synthase in essential hypertension.
abstract: Lipocalin-type prostaglandin D synthase (L-PGDS) reportedly well predicts cardiovascular injuries in humans. However, little is known about the implications of L-PGDS in hypertension. In the present study, we investigated the alterations of serum and urinary L-PGDS in hypertensive patients with or without renal dysfunction. A total of 111 patients with hypertension (EHT; 65 with normoalbuminuria, 23 with microalbuminuria, 12 with macroalbuminuria, 11 with renal failure) and 102 normotensive, nomoalbuminuric subjects (NT) were studied. L-PGDS was measured by enzyme-linked immunosorbent assay, and L-PGDS in the kidney was localized using immunohistochemical methods. Blood pressure was higher in EHT groups than in the NT group (P<0.0001). There were no differences in age, gender, BMI, TC, TG, and HbA1c levels among the groups. Serum creatinine and urinary albumin levels were higher in the group with renal failure. Serum levels of L-PGDS were increased in EHT with normoalbuminuria, as compared with NT (0.88 +/- 0.05 versus 0.65 +/- 0.02 microg/mL; P<0.001). Serum levels of L-PGDS increased with the renal function worsened and positively correlated with serum creatinine, particularly in patients with renal impairments (r=0.76, P<0.0001). Similarly, the urinary L-PGDS excretions in EHT with normoalbuminuria were higher than that in NT (2.31 +/- 0.29 versus 1.16 +/- 0.14 mg/gCr, P<0.001), whereas there were no differences in urinary albumin excretion between the 2 groups. Moreover, urinary L-PGDS excretion increased dramatically with an increase in albuminuria or proteinuria. L-PGDS was stained in the tubules and the interstitium of the kidney in nephrosclerosis. In conclusion, patients with hypertension exhibited a higher level of L-PGDS in serum and urine, and this became increasingly obvious along with advance in renal dysfunction. These data suggest that L-PGDS metabolism is related to blood pressure and kidney injuries associated with hypertension.
authors.affiliation: Department of Medicine 2, Yokohama City University, Japan.
authors.forename: Nobuhito
authors.initials: N
authors.lastname: Hirawa
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Uehara
authors.forename: Minoru
authors.initials: M
authors.lastname: Yamakado
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Toya
authors.forename: Tomoko
authors.initials: T
authors.lastname: Gomi
authors.forename: Toshio
authors.initials: T
authors.lastname: Ikeda
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Eguchi
authors.forename: Masao
authors.initials: M
authors.lastname: Takagi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Oda
authors.forename: Kousuke
authors.initials: K
authors.lastname: Seiki
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Urade
authors.forename: Satoshi
authors.initials: S
authors.lastname: Umemura
mesh_terms: D002352:Carrier Proteins / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000201:enzymology* / Q000652:urine; D007150:Immunohistochemistry; D019746:Intramolecular Oxidoreductases / Q000097:blood / Q000378:metabolism* / Q000652:urine; D007668:Kidney / Q000201:enzymology; D054835:Lipocalin 1; D054834:Lipocalins; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis
chemical_list: D002352:Carrier Proteins; C518443:LCN1 protein, human; D054835:Lipocalin 1; D054834:Lipocalins; D019746:Intramolecular Oxidoreductases; C022466:prostaglandin R2 D-isomerase