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It is well known that coronary events and changes in the fibrinolytic system are common complications seen in end stage renal disease (ESRD) patients. Previous studies have shown that the activities of the enzymes of fibrinolytic pathway differ between normal individuals and ESRD patients. Plasminogen activator inhibitor-1 (PAI-1) enzyme regulates the activity of the fibrinolytic pathway by inhibiting tissue plasminogen activator (t-PA) enzyme. It is postulated that this inhibitory effect differs in ESRD patients. Several previous studies have shown high levels of PAI-1 enzyme in ESRD patients. It has also been shown by these studies that angiotensin-II is responsible from this high levels.
Angiotensin-II, that is a component of reninaldosteron-angiotensin system, is a potent vasoconstrictor and plays an important role in the regulation of vascular tone. Angiotensin Converting Enzyme (ACE) is responsible for the conversion of Angiotensin I to Angiotensin II and it is now known that this enzyme has a genetic profile. Patients who has the D allele has high enzyme activity.
In this study, we planned to determine the relation between PAİ-1 levels and angiotensin converting enzyme (ACE) gene polymorphism.
Our results show that the . PAI 1 levels was statistically higher in ESRD patients compared to healthy controls. However, PAI-1 levels were similar among the subgroups of ACE gene polymorphism. In terms of LDLcholesterol and hematocrit levels there was a positive correlation with PAI-1 levels in ESRD patients.
In conclusion, our results showed that there was no relation between high PAI-1 enzyme levels and ACE gene polymorphism in ESRD patients. We consider that high PAI-1 enzyme levels in these patients can be considered as a risk factor for thrombosis like dislipidemia and high hematocrit levels.