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KRONİK DÎYALÎZ HASTALARINDA ANJÎOTENSÎN DÖNÜŞTÜRÜCÜ ENZÎM GEN POLÎMORFÎZMÎ VE PLAZMÎNOJEN AKTÎVATOR ÎNHÎBÎTÖR-1 ÎLE ÎLÎŞKÎSÎ

ANGIOTENSIN CONVERTING ENZYME GEN POLIMORPHISM AND ITS RELATION WITH PLASMINOGEN ACTIVATOR INHIBITOR-1 IN CHRONIC DIALYSIS PATIENTS

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Abstract (2. Language): 
t 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 renin-aldosteron-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 LDL-cholesterol 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.
Abstract (Original Language): 
Son dönem kronik böbrek yetmezliği (SDBY) olan hastalarda çeşitli kardiyovasküler olaylar ve flbrinolitik sistemde çeşitli değişiklikler görülmektedir. Fibrinolitik sisteme katılan enzimlerin son dönem böbrek yetmezliği olan hastalardaki aktiviteleri ile sağlıklı bireylerdeki aktivitelerinin farklı olduğu tespit edilmiştir. Plazminojen aktivatör inhibitör-1 enzimi (PAİ-1), doku plazminojen aktivatör (t-PA) enzimini inhibe ederek fibrinolitik sistemde bir denge sağlanmasını gerçekleştirimektedir. Bu olayın SDBY olan hastalarda farklı olduğu düşünülmektedir. Bu konuda yapılan çalışmaların sonucunda PAİ-1 seviyesinin bu hastalarda yüksek olduğu saptanmıştır. Yine bu konuda yapılan araştırmalarda PAİ-1 düzeyinin anjiotensin-II etkisi ile yükseldiği saptanmıştır. Anjiotensin-I, renin aldosteron anjiotensin sisteminin bir parçası olup organizmada önemli bir rol oynamaktadır. Anjiotensin-II oluşumunda rol oynayan anjiotensin dönüştürücü enziminin (ADE) bir genetik profilinin var olduğu ve bazı çalışmalarda D aleli olanlarda bu enzim aktivtesinin daha yüksek olduğu gösterilmiştir. Çalışmamızda PAİ 1 aktivitesi ile beraber ADE gen polimorflzimi arasındaki ilişki araştırmayı hedefledik. Aldığımız sonuçlarda hasta gurubunda sağlıklı guruba karşı PAİ-1 seviyesi yüksek tespit edilmiştir ve istatistiksel olarak anlamlı bulunmuştur. ADE gen polimorfızmi alt guruplarında ise aldığımız sonuçların anlamlı olmadığı görüldü. LDL kolesterolü ve hematokrit değerlerinin PAİ-1 ile pozitif korelasyon gösterdiği saptandı. Sonuç olarak SDBY olan hastalarda PAİ-1 enziminin yüksekliği ile ACE gen polimorfızmi arasında bir ilişki saptanamamıştır.Bu hastalardaki PAİ-1 yüksekliğinin dislipidemi ve hematokrit yüksekliği gibi trombotik olaylar açısından bir risk faktörü olarak düşünülebileceği kanısına varıldı.
FULL TEXT (PDF): 
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