Background: Renal impairment (RI) is associated with worse prognosis. Recently, cystatin C has been shown to represent a potentially superior marker of the glomerular filtration rate compared with creatinine clearance (CrCl). We evaluated the impact of cystatin C and other markers of RI on prognosis in a large cohort of patients with coronary heart disease (CHD). Methods: Cystatin C, creatinine (Cr), and CrCl were determined at baseline in a cohort of 1033 patients (30 -70 years) with CHD. Patients were followed for a mean of 33.5 months, and a combined endpoint [fatal and nonfatal cardiovascular disease (CVD) events] was used as the outcome variable. Cystatin C was measured by immunonephelometry, and CrCl was calculated. Results: During follow-up, 71 patients (6.9%) experienced a secondary CVD event. Neither Cr (P ؍ 0.63) nor CrCl (P ؍ 0.10) were associated with incidence of CVD events, whereas cystatin C was clearly associated with risk of secondary CVD events (P <0.0001). In multivariate analyses, patients in the top quintile of the cystatin C distribution at baseline had a statistically significantly increased risk of secondary CVD events even after adjustment for classic risk factors, severity of coronary disease, history of diabetes mellitus, treatment with angiotensin-converting enzyme inhibitors, and Creactive protein (hazard ratio, 2.27; 95% confidence in-
Because dietary intake is supposed to be an important route of human exposure we quantified the dietary intake of perfluorooctane sulfonate (PFOS), perfluorooctanoate (PFOA), perfluorohexane sulfonate (PFHxS), perfluorohexanoate (PFHxA), and perfluorooctane sulfonamide (PFOSA) using 214 duplicate diet samples. The study was carried out with a study population of 15 female and 16 male healthy subjects aged 16-45 years. The participants collected daily duplicate diet samples over seven consecutive days in 2005. Duplicate samples were homogenized and their ultrasonic extracts were cleaned up by SPE and subjected to HPLC-ESI-MS/MS. In addition, individual intakes were estimated based on blood levels of PFOS and PFOA using a pharmacokinetic model. Blood samples were collected once during the sampling period. The median (90th percentile) daily dietary intake of PFOS and PFOA was 1.4 ng/kg b.w. (3.8 ng/kg b.w.) and 2.9 ng/kg b.w. (8.4 ng/kg b.w.), respectively. PFHxS and PFHxA could be detected only in some samples above detection limit with median (maximum) daily intakes of 2.0 ng/kg b.w. (4.0 ng/kg b.w.) and 4.3 ng/kg b.w. (9.2 ng/kg b.w.), respectively. Because PFOSA could not be detected above the limit of detection of 0.2 ng/g f.w. this indirect route of exposure seems to be of less significance. Overall, the results of this study demonstrate that the German population is exposed to PFOS and PFOA, but the median dietary intake did not reach the recommended tolerable daily intake by far. Biomonitoring data predict an exposure in a comparable range. We suppose that, normally, food intake is the main source of exposure of the general population to PFOS and PFOA.
Increased concentrations of Lp-PLA2 predict future cardiovascular events in patients with manifest CHD independent of a variety of potential risk factors including markers of inflammation, renal function, and hemodynamic stress.
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