Hambali Z, Ahmad Z, Arab S, Khazaai H
Department of Pathology, Chemical Pathology Unit, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia.
Indian J Nephrol. 2011 Jan;21(1):21-5. doi: 10.4103/0971-4065.75218.
Cardiovascular disease (CVD) is responsible for the majority of deaths in chronic renal failure (CRF). Oxidative stress plays a key role in pathogenesis of atherosclerosis and CVD, which is promoted by the production of reactive oxygen species (ROS) and impaired antioxidant enzymes. These ROS react with nitric oxide (NO) to produce cytotoxic reactive nitrogen species that cause oxidative injury to the endothelium. This study evaluated biomarkers of oxidative stress, NOx (total NO(2) and NO(3)), and superoxide dismutase (SOD) enzyme in normal control and CRF patients as case group and correlated their association with CVD. This cross sectional study involved 173 CRF patients on different modes of treatment (hemodialysis, continuous ambulatory peritoneal dialysis (CAPD), and predialysis). Of these, 74 had CVD. The control group consisted of 33 healthy subjects who had no history of CRF and CVD. Both NOx and SOD levels were significantly lower (P<0.05, P<0.001, respectively) in the case group. Comparing between CRF patients with and without CVD, SOD level was found to be significantly lower in CRF patients with CVD (P<0.05). Logistic regression analysis showed significant association of CVD event with age, male gender, diabetes, SOD level, and lipid profile in CRF patients. Oxidative stress occurs in the CRF patients with or without CVD. This study found that NOx and SOD levels were reduced in all CRF patients with or without CVD. However, it was noted that the levels of these biomarkers of oxidative stress were significantly lower in CRF patients with CVD compared with CRF patients without CVD. Therefore, these oxidative stress markers maybe contributing factors in the pathogenesis of CVD in patients with CRF.
心血管疾病（CVD）是慢性肾衰竭（CRF）患者死亡的主要原因。氧化应激在动脉粥样硬化和心血管疾病的发病机制中起关键作用，活性氧（ROS）的产生及抗氧化酶受损会加剧氧化应激。这些ROS与一氧化氮（NO）反应生成细胞毒性活性氮，对内皮造成氧化损伤。本研究评估了正常对照组及作为病例组的CRF患者氧化应激生物标志物、氮氧化物（总NO₂和NO₃）和超氧化物歧化酶（SOD）水平，并将它们与心血管疾病的关联进行了相关性分析。这项横断面研究纳入了173例接受不同治疗方式（血液透析、持续性非卧床腹膜透析（CAPD）和透析前）的CRF患者。其中，74例患有心血管疾病。对照组由33名无CRF和心血管疾病病史的健康受试者组成。病例组中氮氧化物和SOD水平均显著降低（分别为P<0.05，P<0.001）。比较有和没有心血管疾病的CRF患者，发现有心血管疾病的CRF患者SOD水平显著更低（P<0.05）。逻辑回归分析显示，心血管疾病事件与CRF患者的年龄、男性性别、糖尿病、SOD水平和血脂谱显著相关。无论是否患有心血管疾病，CRF患者均会发生氧化应激。本研究发现，所有有或没有心血管疾病的CRF患者中氮氧化物和SOD水平均降低。然而，值得注意的是，与没有心血管疾病的CRF患者相比，有心血管疾病的CRF患者中这些氧化应激生物标志物的水平显著更低。因此，这些氧化应激标志物可能是CRF患者心血管疾病发病机制中的促成因素。
