title: C-reactive protein is associated with cigarette smoking-induced hyperfiltration and proteinuria in an apparently healthy population.
abstract: Although cigarette smoking is known to be an important risk factor for renal disease, the mechanism by which smoking induces progressive renal disease in a healthy population has not been established. We hypothesized that oxidative stress (measured as 8-iso-prostaglandin F(2α), 8-iso-PGF2a), inflammation (highly sensitive C-reactive protein (CRP), hs-CRP) and nitric oxide may be associated with an alteration in the estimated glomerular filtration rate (eGFR) and proteinuria in otherwise healthy smokers. A total of 649 eligible subjects were classified according to their smoking status. Plasma NOx was measured using ozone-based chemiluminescence, urinary 8-iso-PGF2a was measured using enzyme immunoassay and serum hs-CRP was measured using a latex aggregation nephelometry method. The levels of 8-iso-PGF2a and hs-CRP increased in current smokers (P=0.001 and P=0.029, respectively), although there was not an increase in the NOx level. The prevalence of a high eGFR increased in light smokers (odds ratio (OR) 1.15 (95% confidence interval (CI), 0.61-2.17)) and heavy smokers (OR 2.33 (95% CI, 1.06-5.10)) when compared with non- and past smokers (P for trend=0.024). The multivariable-adjusted mean values of the eGFR in current smokers, reported from the lowest to the highest quintiles of hs-CRP levels, were 82.1, 85.1, 86.4 and 88.5 ml per min per 1.73 m² (P for trend=0.027). The mean values of proteinuria were 28.6, 34.6, 37.2 and 39.5 mg g⁻¹ creatinine (P for trend=0.003). The correlation coefficient between hs-CRP and eGFR was increased significantly (P=0.03) across non- (r=0.03), past (r=-0.17), light (r=0.13) and heavy smokers (r=0.31). In conclusion, cigarette smoking is a risk factor for renal function alteration in healthy smokers and is characterized by a high eGFR and a high urinary protein associated with an increase in the hs-CRP. This finding suggests that hs-CRP may help mediate the alteration of renal function in smokers.
authors: Department of Public Health, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
authors: Rani
authors: R
authors: Sauriasari
authors: Noriko
authors: N
authors: Sakano
authors: Da-Hong
authors: DH
authors: Wang
authors: Jiro
authors: J
authors: Takaki
authors: Kei
authors: K
authors: Takemoto
authors: BingLing
authors: B
authors: Wang
authors: Hitoshi
authors: H
authors: Sugiyama
authors: Yoshie
authors: Y
authors: Sato
authors: Tomoko
authors: T
authors: Takigawa
authors: Noriko
authors: N
authors: Takahashi
authors: Sakiko
authors: S
authors: Kanbara
authors: Yoshiaki
authors: Y
authors: Hitomi
authors: Hiroyuki
authors: H
authors: Nakamura
authors: Keiki
authors: K
authors: Ogino
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis / Q000502:physiology*; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007674:Kidney Diseases / Q000209:etiology* / Q000503:physiopathology; D007677:Kidney Function Tests; D008019:Life Style; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000097:blood; D011507:Proteinuria / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D012907:Smoking / Q000009:adverse effects / Q000097:blood / Q000503:physiopathology*; D055815:Young Adult
chemical_list: D015415:Biomarkers; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D002097:C-Reactive Protein; D015237:Dinoprost