dc.description.abstract | Chronic kidney failure is a syndrome characterized by progressive and irreversible loss of nephrons due to a miscellany of other diseases. In patients with chronic kidney failure, immune system disorders have been observed, arising from a variety of causes. Prevalence of infections Hepatitis B and C increase in direct proportion to the stage of the disease in hemodialysis patients due to increased immune system disorders in late stages and problems that occur during the treatment. Viruses of Hepatitis B and C, common inflammatory diseases observed in hemodialysis patients, display a function that increases oxidative stress in these patients. The objective of our study was to evaluate in detail using various parameters the oxidative stress developing in patients with chronic kidney failure who receive hemodialysis treatment and are diagnosed with Hepatitis B and C, based on the weakening of the immune system in chronic kidney failure patient groups who receive hemodialysis and the high infection risk of viral diseases during the treatment period. On the basis of this objective, we aimed to determine the levels of 3-Nitrotyrosine inflammation indicator of protein oxidation and TWEAK brought forth as a cell growth inductor and heat shock protein 70 (HSP70) in both ill and healthy patients. As a result, that viral diseases trigger inflammation and that these patients have higher oxidative stress compared to healthy individuals were observed in the light of the gathered data. In our study: Caused partially by hepatitis B and C in addition to hemodialysis treatment in included patients with chronic kidney failure, the effect of oxidative stress on the prognosis of the disease has been demonstrated. Our study bears great significance in its capacity to guide further studies on the same patient groups. | en_US |
dc.description.tableofcontents | İÇİNDEKİLER Sayfa ÖZET , iv ABSTRACT, vi TEŞEKKÜR,viii İÇİNDEKİLER , ix ÇİZELGELER DİZİNİ , xi ŞEKİLLERİN LİSTESİ,xii SİMGELER VE KISALTMALAR,xiii 1. GİRİŞ , 1 2. BÖBREK YETMEZLİĞİ , 4 2.1. Akut Böbrek Yetmezliği , 4 2.1.1 Akut böbrek yetmezliğinin nedenleri , 4 2.1.2. Akut böbrek yetmezliğinin komplikasyonları, 5 2.2. Kronik Böbrek Yetmezliği (KBY), 6 2.2.1. Kronik böbrek hastalığının evreleri, 6 2.2.2. Kronik böbrek yetmezliği patogenezi , 8 2.2.3. Kronik böbrek yetmezliğinde tedavi , 9 3. HEPATİT B , 19 3.1. Patogenez , 19 3.2. Kronik HBV Enfeksiyonunun Doğal Seyri, 20 3.3. Klinik Sendromlar, 21 3.4. Bulaşma Yolları, 24 3.5. Epidemiyoloji, 25 4. HEPATİT C , 27 4.1. Patogenez , 27 4.2. Hepatit C Enfeksiyonunun Doğal Seyri, 28 4.3. Klinik Sendromlar, 29 4.4. Bulaşma Yolları, 30 x Sayfa 4.5. Epidemiyoloji, 31 5. KRONİK BÖBREK YETMEZLİĞİNDE HEMODİYALİZ VE HEPATİT B/C PREVELANSI, 33 6. OKSİDATİF STRES, 35 6.1. Reaktif Oksijen Türleri ve Serbest Radikaller , 35 6.2. Reaktif Oksijen ve Nitrojen Türlerinin Makromoleküller Üzerindeki Etkileri39 6.3. Serbest Radikallere Karşı Hücresel Savunma Sistemleri, 43 6.4. 3-Nitrotirozin (3-NT) , 49 6.5. Kronik Böbrek Yetmezliğinde Oksidatif Stres Ve Antioksidanlar, 52 6.6. Oksidatif Stres ve İnflamasyon İlişkisi , 54 7. TWEAK(Tumor Necrosis factor- Like Weak Inducer of Apoptosis ), 57 8. ISI ŞOK PROTEİNİ: HSP70 , 59 9. MATERYAL VE METOT , 61 9.1. Materyal , 61 9.2. Metot , 63 10. BULGULAR, 68 10.1. 3-Nitrotirozin Sonuçlarının Değerlendirilmesi , 69 10.2. Tweak Sonuçlarının Değerlendirilmesi, 71 10.3. Hsp70 Sonuçlarının Değerlendirilmesi , 73 11. TARTIŞMA , 75 12. SONUÇ, 80 KAYNAKLAR , 82 ÖZGEÇMİŞ , 98 | |