Böbrek nakli yapılan hastalarda, adiponektin, leptin, nitrik oksit, C-reaktif protein düzeyleri ve statin tedavisinin etkileri
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Date
2008
Authors
Ocak, Nihal
Journal Title
Journal ISSN
Volume Title
Publisher
Uludağ Üniversitesi
Abstract
Böbrek nakli (BN) hastalarında kardiyovasküler hastalıklar (KVH) en önemli mortalite ve morbidite nedenidir. BN hastalarında sekonder lipid metabolizma bozuklukları, endotelyal disfonksiyon ve inflamasyon KVH gelisme riskini arttırmaktadır. Bu yüzden bu hasta grubunda lipid düzeylerinin yanı sıra subklinik aterosklerozun erken belirteci olabilecek nitrik oksit (NO), yüksek duyarlılıklı C reaktif protein (hs-CRP), adiponektin ve leptin düzeylerinin incelenmesi yararlı olabilir. Statinlerin lipid düsürücü etkilerinin ötesinde, endotel disfonksiyonunu düzelttigi, inflamasyonu azalttıgı, adiponektin seviyelerini azaltıp leptin seviyelerini arttırdıgı gösterilmistir. Ancak statinlerin BN hastalarındaki etkilerine dair bilgiler sınırlıdır. Bu çalısmada, BN hastalarında takrolimus ve siklosporin‘in; NO, hs- CRP, adiponektin, leptin seviyelerine ve lipid profiline etkisi ve statin tedavisi ile bu parametrelerde görülebilecek degisikliklerin arastırılması planlandı. Ayrıca bu parametreler kronik böbrek yetmezlikli (KBY) hastalar, hemodiyaliz (HD) hastaları ve saglıklı kontroller (SK) ile karsılastırıldı. Her gruba 18 kisi alındı. BN hastaları siklosporin ve takrolimus kullananlar olmak üzere iki alt guruba ayrıldı. Lipid profili, NO, hs-CRP, adiponektin, leptin düzeyleri fluvastatin (80 mg/gün) tedavisi öncesi ve sonrası 6.ayda degerlendirildi. Nitrik oksit ve adiponektin seviyeleri KBY, HD ve BN hastalarında; hs- CRP, HD ve BN hastalarında; leptin düzeyleri, BN hastalarında SK’e göre yüksekti. BN hastalarında statin tedavisi sonrasında lipid profili düzelirken hs- CRP düzeyleri azaldı. Takrolimus tedavisi alan alt grupta adiponektin ve hs- CRP düzeyleri anlamlı olarak azaldı. iii Sonuç olarak, BN hastalarında statin tedavisi lipid profilini düzelterekve inflamatuar süreci baskılayarak KVH gelisimini azaltabilir.
Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in kidney transplant recipients (KTRs). Secondary lipid metabolism disorders, endothelial dysfunction and inflammation enhances the risk of CVD development in KTRs. Beyond investigating lipid profile, it might be useful to examine Nitric Oxide (NO), high sensitive C Reactive Protein (hsCRP), adiponectin and leptin levels which are accepted as early indicators of subclinical atherosclerosis. Beyond their lipid lowering effects, it was shown that statins improve endothelial dysfunction, inhibit inflammation, reduce adiponectin and increase leptin levels. However, knowledge about these subjects is limited in KTRs. The aim of the present study was to investigate the lipid profile, NO, hs-CRP, adiponectin and leptin levels in KTRs treated with tacrolimus or cyclosporin and to observe changes with statin therapy. Furthermore, we compared these parameters with those of the patients with chronic renal failure (CRF), hemodialysis (HD) patients and healthy controls (HC). Eighteen subjects were included in each group. KTRs were receiving cyclosporine or tacrolimus. Lipid profile, NO, hs-CRP, adiponectin and leptin levels were evaluated before and after 6 months fluvastatin treatment (80 mg/day). Compared with the HC, serum NO and adiponectin levels were significantly higher in the CRF, HD and KTRs; hs-CRP levels were significantly higher in the HD and KTRs; leptin levels were significantly higher in the KTRs. Lipid profile improved and hs-CRP levels reduced after statin treatment in the KTRs. Adiponectin and hs-CRP levels were significantly reduced in the tacrolimus treated subgroup. We conclude that statin treatment may reduce the CVD development by improving the lipid profile and supressing inflammatory processes in KTRs.
Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in kidney transplant recipients (KTRs). Secondary lipid metabolism disorders, endothelial dysfunction and inflammation enhances the risk of CVD development in KTRs. Beyond investigating lipid profile, it might be useful to examine Nitric Oxide (NO), high sensitive C Reactive Protein (hsCRP), adiponectin and leptin levels which are accepted as early indicators of subclinical atherosclerosis. Beyond their lipid lowering effects, it was shown that statins improve endothelial dysfunction, inhibit inflammation, reduce adiponectin and increase leptin levels. However, knowledge about these subjects is limited in KTRs. The aim of the present study was to investigate the lipid profile, NO, hs-CRP, adiponectin and leptin levels in KTRs treated with tacrolimus or cyclosporin and to observe changes with statin therapy. Furthermore, we compared these parameters with those of the patients with chronic renal failure (CRF), hemodialysis (HD) patients and healthy controls (HC). Eighteen subjects were included in each group. KTRs were receiving cyclosporine or tacrolimus. Lipid profile, NO, hs-CRP, adiponectin and leptin levels were evaluated before and after 6 months fluvastatin treatment (80 mg/day). Compared with the HC, serum NO and adiponectin levels were significantly higher in the CRF, HD and KTRs; hs-CRP levels were significantly higher in the HD and KTRs; leptin levels were significantly higher in the KTRs. Lipid profile improved and hs-CRP levels reduced after statin treatment in the KTRs. Adiponectin and hs-CRP levels were significantly reduced in the tacrolimus treated subgroup. We conclude that statin treatment may reduce the CVD development by improving the lipid profile and supressing inflammatory processes in KTRs.
Description
Keywords
Böbrek nakli, Nitrik oksit, C reaktif protein, Adiponektin, Leptin, Statin, Kardiyovasküler hastalık, Kidney transplantation, Nitric oxide, C reactive protein, Adiponectin, Cardiovascular disease
Citation
Ocak, N. (2008). Böbrek nakli yapılan hastalarda, adiponektin, leptin, nitrik oksit, C-reaktif protein düzeyleri ve statin tedavisinin etkileri. Yayınlanmamış uzmanlık tezi. Uludağ Üniversitesi Tıp Fakültesi.