Objective-Increased risk of cardiovascular disease in patients with chronic renal failure (CRF) has been explained by accelerated atherosclerosis and impaired angiogenesis, in which endothelial progenitor cells (EPCs) may play key roles. We hypothesized that altered EPC biology may contribute to the pathophysiology of CRF. Methods and Results-EPCs were isolated from CRF patients on maintenance hemodialysis (nϭ44) and from a normal control group (nϭ30). CRF patients showed markedly decreased numbers of EPC (44.6%) and colonies (75.3%) when compared with the controls (PϽ0.001). These findings were corroborated by 30.5% decrease in EPC migratory function in response to vascular endothelial growth factor (VEGF) (Pϭ0. T he lifespan of patients with chronic renal failure (CRF) is reduced, and coronary artery disease is the most important cause of morbidity and mortality in these patients. 1,2 Even the results of therapeutic strategies such as percutaneous coronary intervention and bypass surgery have shown poor procedural success rates and dismal long-term eventfree survival in CRF patients. 3,4 Most of the increased cardiovascular morbidity and mortality in CRF has been accounted for by the rapid progression of atherosclerosis, which is clinically shown to be accelerated in CRF. 5,6 Experimental studies have also shown that even mild renal dysfunction causes a dramatic acceleration of atherosclerosis. 7 Angiogenesis, which is an essential compensation for myocardial ischemia, is also impaired in CRF. 8 However the mechanism underlying the acceleration of atherosclerosis and impaired angiogenesis by CRF has not been examined closely. Although the phenomenon has been partially explained by the higher prevalence of established risk factors in CRF, such as hypertension, abnormal carbohydrate metabolism, and increased low density lipoprotein (LDL) cholesterol, the extent and severity of cardiovascular disease is clearly disproportionately high relative to the underlying risk factor profile. 9,10 Recent studies have identified that normal adults have a small amount of circulating endothelial progenitor cell (EPC) in the peripheral blood. In response to cytokine stimulation and ischemic insult, these cells are mobilized from bone marrow, home to the ischemic tissue, and contribute to neovascularization and angiogenesis. 11-14 Moreover, EPC is regarded to have a key role in the maintenance of vascular integrity and to act as "repair" cells in response to the endothelial injury, 15,16 which has been regarded as an initial step in atherosclerosis and a result of the actions of various cardiovascular risk factors. 17 Current data suggest that decrease in circulating EPC contributes not only to impaired angiogenesis but also to the progression of atherosclerosis, 18 and patients at risk for coronary artery disease have a decreased number of circulating EPC with impaired activity. 19 -22 Therefore, we reasoned that EPC, which is critical for neovascularization and the maintenance of vascular integrity, Methods Study SubjectsWe...

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Abstract-Serum uric acid is associated with cardiovascular disease. However, the independent role of uric acid in the development of cardiovascular disease is uncertain. This study examined the cross-sectional association of serum uric acid level with microalbuminuria among 6771 subjects without diabetes or hypertension. Blood pressure was categorized as prehypertension (systolic blood pressure, 120 to 140 mm Hg or diastolic blood pressure, 80 to 90 mm Hg) and normotension (systolic blood pressure, Ͻ120 mm Hg and diastolic blood pressure, Ͻ80 mm Hg). Microalbuminuria was found in 4.0% of normotensive subjects (nϭ4819) and in 7.9% of prehypertensive subjects (nϭ1952 006).However, the difference in serum uric acid level according to the presence or absence of microalbuminuria was not found in the normotensive group. Multiple logistic regression models showed that, in the prehypertensive group, after adjustment for other cardiovascular risk factors, the highest uric acid quartile entailed Ͼ2 times greater risk for microalbuminuria than the lowest quartile in both men (odds ratio, 2.12; 95% CI, 1.16 to 3.87) and women (odds ratio, 3.36; 95% CI, 1.17 to 9.69). In the normotensive group, serum uric acid quartile did not show the independent association with microalbuminuria. In conclusion, serum uric acid level was strongly associated with microalbuminuria in prehypertensive subjects.