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Kinetics of tissue plasminogen activator in cerebrospinal fluid, serum and urine of 12 patients with severe acute brain injury was evaluated to test the hypotheses that the activity of this enzyme is exclusively due to a combined effect of its tissue origin and its vascularization by means of the blood-brain barrier. Infusion of thrombin induces a progressive decrease of tissue plasminogen activator into the extravascular space paralleling the decrease of plasminogen activator inhibitor-1. However, it was observed that there is an early increase of tissue plasminogen activator into the cerebrospinal fluid of two patients. This was followed by a decrease that parallels that of serum plasminogen activator inhibitor-1. Neither has an increase of the activity of this enzyme in the urine of the same patients. These data provide evidence that in the studied conditions, the increase of t-PA activity in the cerebrospinal fluid corresponds to a tissue origin. However, it cannot be excluded that in these 2 cases, it could be related to some degradation of plasminogen activator inhibitor-1.Risk stratification in the asymptomatic on hemodialysis patients.

Dialysis patients, especially the asymptomatic ones, are in a state of medical risk. This study was undertaken to stratify the risk of cardiovascular events and malnutrition status in asymptomatic patients. This retrospective cohort study was carried out on 412 asymptomatic patients receiving hemodialysis in a tertiary hospital in central Taiwan. The participants’ demographic characteristics, clinical