Impact of cystatin C levels on infarct size and hemorrhage volume in acute cerebral stroke.
ABSTRACT Studies have indicated that serum levels of cystatin C (a sensitive marker of renal function) are significantly associated with cerebral vascular events. However, the influence of cystatin C on infarct size and hemorrhage volume in acute cerebral stroke has not been well established. A total of 222 patients with cerebral infarction, and 69 patients with cerebral hemorrhage, as well as 122 healthy controls were included in this study. Patients were further divided into subgroups according to infarct size and hemorrhage volume. Serum levels of cystatin C were significantly higher in cerebral-stroke patients than healthy controls (p < 0.05). Logistic multiple regression analyses showed that cystatin C levels were correlated with ischemic stroke and hemorrhagic cerebral stroke (p < 0.01). Cystatin C levels were correlated only with age, urea level, and creatinine level (p < 0.05). There was no correlation between cystatin C levels and systolic blood pressure, diastolic blood pressure, as well as levels of fasting blood glucose, triglyceride, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol (p > 0.05). Patients with larger infarcts or larger hemorrhage volumes had higher levels of cystatin C (p < 0.05). Certain factors affect cystatin C levels in cerebral-stroke patients, and they could be considered to be independent predictors of infarct size and hemorrhage volume in acute cerebral stroke events.
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ABSTRACT: Abstract Renal dysfunction is associated with mortality in patients after ischemic stroke. Cystatin C is a potentially superior marker of renal function compared to creatinine and estimated glomerular filtration rate (GFR). In our observational cohort study, 390 Caucasian patients suffered from acute ischemic stroke (mean age 70.9 years; 183 women and 207 men) were included and prospectively followed up to maximal 56 months. Serum creatinine and cystatin C were measured at admission to the hospital; GFR was estimated according to CKD-EPI creatinine and CKD-EPI creatinine/cystatin equations. According to values of serum creatinine, estimated GFR and serum cystatin C patients were divided into quintiles. In the follow-up period, 191 (49%) patients died. For serum cystatin C and estimated GFR based on creatinine and cystatin C, the mortality and the hazard ratios for long-term mortality increased from the first to the fifth quintile nearly linearly. The associations of serum creatinine and estimated GFR categories based on creatinine with long-term mortality were J-shaped. As compared with lowest quintile of serum cystatin C, the fifth quintile was associated with long-term mortality significantly also after multivariate adjustment (age, gender, initial stroke severity, known risk factors for stroke mortality). In contrast, in adjusted analysis serum creatinine and estimated GFR (CKD-EPI creatinine and CKD-EPI creatinine/cystatin) were not associated with long-term mortality. In summary, serum cystatin C was independently and better associated with the risk of long-term mortality in patients suffering from ischemic stroke than were creatinine and estimated GFR using both CKD-EPI equations.Renal Failure 09/2013; · 0.94 Impact Factor