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: Cystatin C (CysC) has been used as a renal function indicator and a strong predictor of cardiovascular events. In this study, we determined the prognostic value of serum CysC in patients with acute ischemic stroke (AIS) and examined its protective role on ischemic brain injury. First-ever stroke patients (601 cases) and control subjects (325 cases) were recruited. Serum CysC level in patients with AIS were significantly higher than that in controls. Multivariate logistic regression analyses showed that elevated CysC is an independent risk factor of AIS; the odds ratio (95 % confidence interval) was 9.80 (3.12-30.83). The integrated population was divided into quintiles according to serum CysC. Compared with the first quintile, the odds ratios of risk for AIS in fourth quintile and fifth quintile were 1.92 (1.08-3.40) and 2.88 (1.49-5.54), respectively. Serum CysC was not associated with neurological deficits and the location of ischemic area; however, serum CysC in patients decreased after one-week therapy. This was consistent with CysC expression after ischemia/reperfusion injury in a mouse focal ischemia/reperfusion injury model. Exogenous CysC exerted neuroprotective effects by reducing infarct volume in this animal stroke model. Therefore, serum CysC is highly associated with AIS and is an independent prediction marker for AIS. Since our findings demonstrated the protection of exogenous CysC on ischemic brain injury, CysC is a novel and promising therapeutic target for AIS.Neurotoxicity Research 02/2015; 28(1). DOI:10.1007/s12640-015-9522-3 · 3.15 Impact Factor
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ABSTRACT: The aim of this study was to investigate the changes in the levels of cystatin C, which protects neurodegeneration in the central nervous system with the inhibition of cysteine protease and by inducing autophagy in the pathogenesis of cerebral vasospasm and levels of vasoconstrictive neuropeptid Y (NPY) in the brain tissue homogenates of rat model of subarachnoid hemorrhage (SAH). Three experimental groups were used: Day 2 and Day 7 groups after SAH, and also a control group. There were seven Wistar albino rats in each group. SAH was accomplished by transclival basilar artery puncture. Rat cystatin C, rat NPY were determined with ELISA in brain tissue homogenates. Day 2 group showed significantly enhanced cystatin C values in comparision with the control group (P=0.048). NPY levels between the Day 2 and Day 7 groups and the control groups were not significantly different (P=0.315). In histopathological examination, there was less neuronal loss in the Day 2 group than in the Day 7 group. Regarding our results, it would be more valuable to measure NPY levels in specific brain areas. The increased cystatin C levels on the second day after SAH is probably a pathophysiologic mechanism to organize protease activity.Acta biochimica Polonica 12/2014; 61(4). · 1.39 Impact Factor
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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; DOI:10.3109/0886022X.2013.832314 · 0.78 Impact Factor