OBJECTIVE—Albuminuria can be caused by endothelial dysfunction as a result of ischemic nephropathy rather than classic diabetic nephropathy. We studied whether renal vascular resistance (resistive index [RI]) of the main renal arteries could be associated with albuminuria and further assessed the relationship between RI and aorta stiffness measured by brachial-ankle pulse-wave velocity (baPWV). RESEARCH DESIGN AND METHODS—We consecutively studied 150 patients with type 2 diabetes and the absence of clinically overt renal artery stenosis. Renal function expressed as the estimated glomerular filtration rate (eGFR) was calculated using the modified formula of modification of diet in renal disease (MDRD). The RI [(peak systolic velocity –end-diastolic velocity)/peak systolic velocity] was measured with duplex Doppler ultrasonography. RESULTS—When the presence of albuminuria (uAlb) was defined as urinary albumin-to-creatinine ratio (μg/mg · creatinine) >30, mean RI [(left RI + right RI)/2] was significantly higher in uAlb, compared with that in patients without uAlb. RI had significant associations with age (r = 0.398, P < 0.0001), diastolic blood pressure (r = −0.398, P < 0.0001), eGFR (r = −0.373, P < 0.0001), and baPWV (r = 0.223, P < 0.05), respectively. Multivariate logistic regression analysis showed that increased RI when defined as RI >0.72 (median) was significantly associated with age (P < 0.01, 95%CI 1.02–1.19), diastolic blood pressure (P < 0.01, 0.86–0.97), and uAlb (P < 0.01, 1.53–15.46), respectively. Moreover, RI was an independent risk factor for uAlb after adjustment of both diastolic blood pressure and eGFR. CONCLUSIONS—Renal vascular resistance was associated with albuminuria and aorta stiffness. Increased RI may imply the presence of any type of underlying renal damage, including ischemic nephropathy.

Endothelial progenitor cells (EPCs) are currently being studied as candidate cell sources for revascularization strategies. Despite these promising results, widespread clinical acceptance of EPCs for clinical therapies remains hampered by several challenges. The challenges and issues surrounding the use of EPCs and the current paradigm being developed to improve the harvest efficiency and functionality of EPCs for application in regenerative medicine are discussed. It has been observed that controversies have emerged regarding the isolation techniques and classification and origin of EPCs. This manuscript attempts to highlight the concept of EPCs in a sequential manner, from the initial discovery to the present (origin, sources of EPCs, isolation, and identification techniques). Human and murine EPC marker diversity is also discussed. Additionally, this manuscript is aimed at summarizing our current and future prospects regarding the crosstalk of EPCs with the biology of hematopoietic cells and culture techniques in the context of regeneration-associated cells (RACs).

Background and objectives: It is known that coronary artery calcification (CAC) develops in chronic kidney disease (CKD) before initiation of renal replacement therapy, and factors associated with CKD mineral and bone disorders (CKD-MBDs) are involved. However, little information is available about any association between plasma levels of asymmetric dimethylarginine (ADMA), insulin resistance, and CAC. Design, setting, participants, & measurements: A total of 111 CKD patients (79 men, 32 women; glomerular filtration rate [GFR] median, 33.7 ml/min per 1.73 m²), free of cardiovascular disease, were consecutively recruited along with 30 age-matched healthy subjects. Coronary artery calcification scores (CACS) were measured by multidetector-row CT according to Agatston score. Results: In CKD patients, CACS was distributed widely from 0 to 2901, while in age-matched, healthy control subjects (n = 30), CACS showed a range from 0 to 307. GFR had a significant negative correlation with CACS. Plasma ADMA levels were negatively correlated with GFR and positively correlated with CACS. When CACS was divided into quartiles (600, n = 17), the patients with CACS >600 had significantly higher values of HOMA-IR, plasma ADMA levels, and fibrinogen along with serum levels of phosphorus, compared with those in patients having CACS <50. Multivariate regression analysis determined HOMA-IR as an independent contributing factor to CACS. Conclusions: CAC becomes more prevalent and severe with a decline in GFR, and plasma ADMA levels and insulin resistance, independent of factors associated with CKD-MBD, are correlated with CAC.