The prevalence of coronary artery stenosis (CAS) at the initiation of renal replacement therapy (RRT) in patients with chronic kidney disease (CKD) and no previous history of angina and/or myocardial infarction (MI) has not been fully elucidated. The prevalence of significant CAS was evaluated in 30 asymptomatic stage 5 CKD patients without a history of angina and/or MI by coronary angiography at the initiation of RRT. The correlations of various parameters with the prevalence of CAS were also examined. Atherosclerotic surrogate markers, including intima-media thickness of carotid artery and ankle-brachial BP index (ABI), were also evaluated. Significant CAS (>50% stenosis) was seen in 16 (53.3%) of 30 asymptomatic CKD patients on coronary angiography at the start of RRT. Stress cardiac scintigraphy was not effective for detecting hidden cardiac ischemia among the CKD patients. Univariate analysis showed that diabetes (P ؍ 0.01), left ventricular mass index (P ؍ 0.04), hyperlipidemia (P ؍ 0.04), total cholesterol (P ؍ 0.02), LDL cholesterol (P < 0.01), intima-media thickness (P ؍ 0.04), and fibrinogen (P ؍ 0.01) were positively correlated with the presence of CAS, whereas ABI (P < 0.01) showed a negative correlation with CAS. Stepwise logistic regression analysis revealed that diabetes and fibrinogen were significant and independent risk factors for CAS in asymptomatic CKD patients who started RRT. The results clearly demonstrated that despite the absence of cardiac events, stage 5 CKD patients are already in a very high risk group for CAS at the initiation of RRT, which was also closely associated with a significant decrease in ABI.
Present quantitative analysis clearly provided the first evidence that arterial calcification of lower limbs' arteries was closely associated with the prevalence and severity of PAD in HD patients. Furthermore, arterial calcification of below-knee arteries and micro-inflammation represented as CRP were the independent associating factors for low TBI, which was the independent associating factor for PAD and CLI in HD patients.
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-tocreatinine ratio (g/mg ⅐ creatinine) Ͼ30, mean RI [(left RI ϩ right RI)/2] was significantly higher in uAlb, compared with that in patients without uAlb. RI had significant associations with age (r ϭ 0.398, P Ͻ 0.0001), diastolic blood pressure (r ϭ Ϫ0.398, P Ͻ 0.0001), eGFR (r ϭ Ϫ0.373, P Ͻ 0.0001), and baPWV (r ϭ 0.223, P Ͻ 0.05), respectively. Multivariate logistic regression analysis showed that increased RI when defined as RI Ͼ0.72 (median) was significantly associated with age (P Ͻ 0.01, 95%CI 1.02-1.19), diastolic blood pressure (P Ͻ 0.01, 0.86 -0.97), and uAlb (P Ͻ 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.
These findings suggest that vitamin E-bonded hemodialyzer is very useful for improving atherosclerosis from a clinical point of view. As one of the underlying mechanisms, as well as antioxidant effects, we want to address an important role of the improvement of rheology of circulating RBCs, which may also help to reduce the requirement of EPO dose in the treatment of anemia of ESRD patients.
Acute kidney disease (AKD), or renal dysfunction persisting >7 days after an initiating event of acute kidney injury, is a rising concern. This study aimed to elucidate the clinical course of AKD after cardiac surgery with data on post-cardiac surgery patients admitted to intensive care units (ICU) at 18 Japanese hospitals during 2012-2014. Using multivariable logistic models, we evaluated the association of AKD with 90-day mortality and the 50% eGFR decline during 2-year follow-up compared to eGFR at 90 days. AKD was defined as an elevation in serum creatinine to at least 1.5-fold from baseline in >7 days after ICU admission. Of the 3,605 eligible patients undergoing cardiac surgery, 403 patients (11.2%) had AKD. Multivariable analysis revealed that the adjusted odds ratio (OR) of AKD for 90-day mortality was 63.0 (95% confidence interval [CI], 27.9-180.6). In addition, the adjusted OR of AKD for 50% eGFR decline was 3.56 (95% CI, 2.24-5.57) among hospital survivors. In conclusion, AKD after cardiac surgery was associated with higher 90-day mortality and renal function decline after hospital discharge.It is well known that acute kidney injury (AKI) is a significant risk of developing subsequent proteinuria and chronic kidney disease (CKD) 1,2 . AKI and CKD seem to be separate conceptualized models because AKI refers to a clinical syndrome characterized by a rapid decrease in renal function while CKD refers to the presence of kidney damage or decreased kidney function for three months or more 3,4 . However, recent studies show that AKI and CKD are not always discrete and can form a continuum with patients who have a sustained renal dysfunction, having an increased risk of developing de novo CKD or deteriorating underlying CKD 5 .Acute kidney disease (AKD), a condition in which renal dysfunction persists over seven days or more after an exposure, is a rising concern because it could play a key role in AKI to CKD transition 6-8 . The term AKD describes the clinical course of acute or subacute damage and/or loss of renal function for a duration of between 7 and 90 days after an AKI-initiating event 6,7 . It is considered that AKD is mostly a consequence of AKI in patients whose renal function is not fully recovered within seven days and progresses to CKD if the AKD is not fully recovered 6,7 . However, the trajectory of AKD remains poorly elucidated.Cardiac surgery-associated AKI (CSA-AKI) is the second most common type of AKI (next to septic shock) and is associated with high in-hospital mortality 9,10 . In addition, CSA-AKI is proven to be a risk for CKD [11][12][13] . Among the characteristics of CSA-AKI are the various timings of occurrence (early or late phase after cardiac surgery) and the various clinical courses (transient or persistent renal dysfunction) due to the complex pathophysiology of CSA-AKI, which includes hemodynamic instability, mechanical stress such as cardiopulmonary bypass, inflammation, oxidative stress, neurohormonal factors, nephrotoxic agents and postoperative complications such as infect...
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