Kwiatkowska Marlena, Oldakowska-Jedynak Urszula, Wojtaszek Ewa, Glogowski Tomasz, Malyszko Jolanta
Department of Nephrology, Dialysis & Internal Diseases, The Medical University of Warsaw, Poland.
Oxid Med Cell Longev. 2021 Feb 20;2021:6660846. doi: 10.1155/2021/6660846. eCollection 2021.
Chronic kidney disease is a public health problem that, depending on the country, affects approximately 8-13% of the population, involving both males and females of all ages. Renal replacement therapy remains one of the most costly procedures. It is assumed that one of the factors influencing the course of chronic kidney disease might be oxidative stress. It is believed that the main mediators of oxidative stress are reactive oxygen species (ROS). Transiently increased concentrations of ROS play a significant role in maintaining an organism's homeostasis, as they are part of the redox-related signaling, and in the immune defense system, as they are produced in high amounts in inflammation. Systemic oxidative stress can significantly contribute to endothelial dysfunction along with exaggeration of atherosclerosis and development of cardiovascular disease, the leading cause of mortality in patients with kidney disease. Moreover, the progression of chronic kidney disease is strictly associated with the atherosclerotic process. Transplantation is the optimal method for renal replacement therapy. It improves better quality of life and prolongs survival compared with hemodialysis and peritoneal dialysis; however, even a successful transplantation does not correct the abnormalities found in chronic kidney disease. As transplantation reduces the concentration of uremic toxins, which are a factor of inflammation per se, both the procedure itself and the subsequent immunosuppressive treatment may be a factor that increases oxidative stress and hence vascular sclerosis and atherosclerotic cardiovascular disease. In the current work, we review the effect of several risk factors in kidney transplant recipients as well as immunosuppressive therapy on oxidative stress.
慢性肾脏病是一个公共卫生问题，根据国家不同，约影响8%-13%的人口，涉及所有年龄段的男性和女性。肾脏替代治疗仍然是最昂贵的治疗手段之一。据推测，影响慢性肾脏病病程的因素之一可能是氧化应激。据信，氧化应激的主要介质是活性氧（ROS）。ROS浓度的短暂升高在维持机体稳态中起重要作用，因为它们是氧化还原相关信号传导的一部分，在免疫防御系统中也起作用，因为它们在炎症中大量产生。全身性氧化应激可显著导致内皮功能障碍，同时加剧动脉粥样硬化和心血管疾病的发展，而心血管疾病是肾脏病患者死亡的主要原因。此外，慢性肾脏病的进展与动脉粥样硬化过程密切相关。移植是肾脏替代治疗的最佳方法。与血液透析和腹膜透析相比，它能改善生活质量并延长生存期；然而，即使移植成功，也无法纠正慢性肾脏病中发现的异常情况。由于移植降低了尿毒症毒素的浓度，而尿毒症毒素本身就是炎症的一个因素，手术本身以及随后的免疫抑制治疗都可能是增加氧化应激从而导致血管硬化和动脉粥样硬化性心血管疾病的一个因素。在当前的工作中，我们综述了肾移植受者的几种危险因素以及免疫抑制治疗对氧化应激的影响。
