Is asymmetric dimethylarginine associated with being born small and large for gestational age? Antioxid Redox Signal. 2014 May 20;20(15):2317-22 Low and high birth weights have been linked to increased susceptibility to cardiovascular and metabolic alterations. However, the natural history of cardiometabolic disturbances in children born small (SGA) and large (LGA) for gestational age is still unclear and no reliable biomarker of cardiovascular risk has definitively been identified in these subjects. Interestingly, asymmetric dimethylarginine (ADMA), antagonist of nitric oxide (NO) production, has been recognized as novel cardiovascular marker able to identify subjects at higher risk of health disturbances. Despite the well-described role of ADMA as a predictor of degenerative disease in adults, its potential application in pediatrics, and specifically in SGA and LGA children, has not been explored as only few data in preterm infants and SGA newborns are available. Therefore, we investigated potential alterations in circulating ADMA and NO levels in SGA and LGA children compared with those born appropriate (AGA) for gestational age. Of note, ADMA was significantly higher in SGA and LGA children than AGA peers. Intriguingly, SGA and LGA categories as well as insulin resistance were independently related to ADMA. Our observations lead to the intriguing hypothesis that ADMA could be involved in the development of cardiometabolic alterations in SGA and LGA children already during the prepubertal age.
Kidney Function and the Risk of Cardiovascular Disease in Patients With Type 2 Diabetes Kidney Int. 2014;85(5):1192-1199. The association of estimated glomerular filtration rate (GFR) with cardiovascular disease risk among patients with type 2 diabetes is unclear. Here we prospectively investigated the race-specific association of estimated GFR with the risk of coronary heart disease and stroke among 11,940 Caucasian and 16,451 African-American patients. During mean follow-up of 6.1–6.8 years, 6647 coronary heart disease and 2750 stroke incident cases were identified. Age- and sex-adjusted hazard ratios of coronary heart disease associated with baseline estimated GFR (90 or more, 75–89, 60–74, 30–59, and 15–29 ml/min per 1.73 m2) were 1.00, 1.04, 1.13, 1.37, and 2.07 (significant trend) for African Americans, and 1.00, 1.09, 1.10, 1.31, and 2.18 (significant trend) for Caucasians, respectively. A significantly increased stroke risk was observed among both African-American and Caucasian participants with an estimated GFR under 60 ml/min per 1.73 m2. When using the updated mean values of estimated GFR, these significant associations became stronger. Participants with mildly decreased estimated GFR (60–89 ml/min per 1.73 m2) during follow-up were also at a significantly higher risk of coronary heart disease and stroke. Thus, even mildly reduced estimated GFR at baseline (under 75 ml/min per 1.73 m2) and during follow-up (under 90 ml/min per 1.73 m2) increased the risk of incident coronary heart disease and stroke among both African-American and Caucasian type 2 diabetes patients. Chronic kidney disease (CKD) and diabetes independently increase cardiovascular disease (CVD) risk.[1,2] Approximately 40% of patients with diabetes develop CKD, manifested as albuminuria, impaired estimated glomerular filtration rate (eGFR), or both.[2,3] Compared with people without diabetes, those with diabetes are already at a high risk for CVD,[4] and the additional development of diabetic kidney disease greatly increases their risk for CVD.[3,5] Studies have found a significant association between the severity of CKD (assessed by eGFR) and CVD risk among the general population[6–9] and among multiple high-risk patient populations, with existing CVD, heart failure, diabetes, and hypertension.[1,5,10,11] However, most studies only provided a single value of eGFR, which may produce potential bias in understanding the magnitude of the association of CKD with incident CVD. Moreover, few studies have addressed the race-specific association of kidney function with the risk of coronary heart disease (CHD) and stroke among diabetic patients, although there are significant racial differences in the prevalence of diabetes in the general population and in the prevalence of end-stage renal disease among diabetic patients.[12,13] This study aims to assess the race-specific association of kidney function with the risk of CHD and stroke among type 2 diabetes patients within the Louisiana State University Hospital–Based Longitudinal Study.
Although the mechanism behind the association between impaired kidney function and the risk of incident CVD is not completely understood, several mechanisms have been proposed. Traditional CVD risk factors, such as older age, smoking, hypertension, and dyslipidemia, often coexist with CKD,[1,2,17] and the positive association of these factors with incident CVD was well documented.[18–20] Elevated asymmetric dimethyl arginine, reduced nitric oxide bioavailability, and endothelial dysfunction in renal disease, which are associated with atherosclerosis, are also recognized as factors linking impaired kidney function and the risk of incident CVD.[21,22] Furthermore, inflammatory markers such as C-reactive protein, fibrinogen, interleukin-6, tumor necrosis factor α, factor VIIc, factor VIIIc, plasmin–antiplasmin complex, D-dimer, and the adhesion molecules E-selection, vascular cell adhesion molecule 1, and Intercellular Adhesion Molecule 1 are often elevated, and the activation of the renin–angiotensin system, which may partly depend on the adaptation to loss of renal mass that results in changes in renal hemodynamics, frequently occurs in CKD. These factors may alter the progression of atherosclerosis through their contribution to the production of reactive oxygen species.[21,23] Besides, increased promoters of calcification and reduced inhibitors of calcification may partly be responsible for the linkage between kidney dysfunction and CVD risk.[21,24] As to eGFR, factors including activation of the renin–angiotensin system, anemia, elevated asymmetric dimethyl arginine, and hyperhomocysteinemia could represent a link between reduced eGFR and increased CVD risk.[22,23,25,26]
Supplementation of folic acid and vitamin B12 reduces plasma levels of asymmetric dimethylarginine in patients with acute ischemic stroke. J Clin Neurosci. 2014 May 6. Increased levels of asymmetric dimethylarginine (ADMA) have been observed in patients with acute ischemic stroke. We aimed to investigate the correlation between ADMA and ischemic stroke, and evaluate the effect of supplementation of folic acid and vitamin B12 on concentrations of ADMA. Patients were randomized into intervention and non-intervention groups within 3days after symptom onset. Intervention group patients were treated with folic acid (5mg daily) and vitamin B12 (500μg twice daily) for 12weeks. ADMA and homocysteine (Hcy) concentrations were measured before treatment (baseline) and 2 and 12weeks after treatment. The laboratory measures were also collected from healthy controls. Eighty five subjects were enrolled in this study, from whom 72 with complete baseline and follow-up laboratory data were included in the present analysis. Thirty four patients were assigned to the intervention group and 38 patients to the non-intervention group. Sixty people were enrolled as healthy controls. Levels of ADMA and Hcy were raised (p<0.05) in patients with acute ischemic stroke. With supplementation of both folic acid and vitamin B12, the levels of ADMA and Hcy decreased significantly at 2 and 12weeks (p<0.05). The present study reconfirmed that ADMA can be regarded as a risk biomarker for acute ischemic stroke. We observed that with supplementation of folic acid and vitamin B12, levels of ADMA were decreased in patients with acute ischemic stroke.
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