Lysophosphatidylcholine, Oxidized Low-Density Lipoprotein and Cardiovascular Disease in Korean Hemodialysis Patients: Analysis at 5 Years of Follow-up

Although oxidized low-density lipoprotein (LDL) and lysophosphatidylcholine (LPC) have been proposed as important mediators of the atherosclerosis, the long-term contribution to the risk of cardiovascular disease (CVD) in hemodialysis patients has not been evaluated. This study investigated the relation between oxidized LDL and LPC levels with long term risk of CVD. Plasma oxidized LDL and LPC levels were determined in 69 Korean hemodialysis patients as a prospective observational study for 5 yr. During the observation period, 18 cardiovascular events (26.1%) occurred including 6 deaths among the hemodialysis patients. The low LPC level group ( 254 microM/L) (P = 0.01). However, serum levels of oxidized LDL were not significantly different between groups with and without CVD. In adjusted Cox analysis, previous CVD, (hazard ratio [HR], 5.68; 95% confidence interval [CI], 1.94-16.63, P = 0.002) and low LPC level (HR, 3.45; 95% CI, 1.04-11.42, P = 0.04) were significant independent risk factors for development of CVD. It is suggested that low LPC, but not oxidized LDL, is associated with increased risk of CVD among a group of Korean hemodialysis patients.

Causal link between oxidative stress, inflammation, and hypertension

Hypertension [HTN] is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. Oxidative stress and its constant companion, inflammation, play a critical part in the pathogenesis of many acute and chronic illnesses including HTN and its long-term complications. There is compelling evidence that oxidative stress, inflammation, and HTN are involved in a self-perpetuating vicious cycle which, if not interrupted, culminates in progressive target organ injury and dysfunction. This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. In addition, evidence will be presented to demonstrate the role of HTN in the pathogenesis of oxidative stress and inflammation. Finally, evidence for participation of tissue angiotensin system in the vicious cycle of oxidative stress, inflammation, and HTN will be presented, and the approach to treatment of HTN-associated oxidative stress will be discussed