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      Clinical Considerations for the Association between Vascular Damage and Chronic Kidney Disease

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          Chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease. Recently, noninvasive and simple morphological and functional methods have been introduced to assess atherosclerotic vascular damage. This review describes the association of CKD with vascular damage as assessed by these methods. Carotid intima-media thickness (IMT) and coronary artery calcium score (CACS) are morphological parameters of vascular damage, and an ankle-brachial index (ABI) <0.90 suggests the presence of peripheral arterial disease (i.e., it represents advanced atherosclerosis). Several prospective studies have demonstrated that CKD is a risk factor for an increased IMT, an increased CACS and a decreased ABI. While it has not been clarified whether measuring the IMT or CACS might be useful to predict the progression of renal function decline, a reduced ABI has been demonstrated as a predictor of accelerated renal function decline. On the other hand, pulse wave velocity (PWV) is a marker of arterial stiffness rather than atherosclerosis, reflecting functional abnormalities caused by vascular damage, and moderate-to-severe CKD may be a risk factor for the progression of arterial stiffness. The measurement of functional markers, especially of PWV or pulse pressure, has been demonstrated to be useful to predict the rate of progression of renal function decline. Thus, renal dysfunction and atherogenic states may be components of a vicious cycle, and vascular function abnormalities associated with atherosclerosis may accelerate this cycle. As the next step, we propose to examine whether improvement of vascular function abnormalities can interrupt this vicious cycle.

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          Most cited references 47

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          Associations of kidney disease measures with mortality and end-stage renal disease in individuals with and without diabetes: a meta-analysis.

          Chronic kidney disease is characterised by low estimated glomerular filtration rate (eGFR) and high albuminuria, and is associated with adverse outcomes. Whether these risks are modified by diabetes is unknown. We did a meta-analysis of studies selected according to Chronic Kidney Disease Prognosis Consortium criteria. Data transfer and analyses were done between March, 2011, and June, 2012. We used Cox proportional hazards models to estimate the hazard ratios (HR) of mortality and end-stage renal disease (ESRD) associated with eGFR and albuminuria in individuals with and without diabetes. We analysed data for 1,024,977 participants (128,505 with diabetes) from 30 general population and high-risk cardiovascular cohorts and 13 chronic kidney disease cohorts. In the combined general population and high-risk cohorts with data for all-cause mortality, 75,306 deaths occurred during a mean follow-up of 8·5 years (SD 5·0). In the 23 studies with data for cardiovascular mortality, 21,237 deaths occurred from cardiovascular disease during a mean follow-up of 9·2 years (SD 4·9). In the general and high-risk cohorts, mortality risks were 1·2-1·9 times higher for participants with diabetes than for those without diabetes across the ranges of eGFR and albumin-to-creatinine ratio (ACR). With fixed eGFR and ACR reference points in the diabetes and no diabetes groups, HR of mortality outcomes according to lower eGFR and higher ACR were much the same in participants with and without diabetes (eg, for all-cause mortality at eGFR 45 mL/min per 1·73 m(2) [vs 95 mL/min per 1·73 m(2)], HR 1·35; 95% CI 1·18-1·55; vs 1·33; 1·19-1·48 and at ACR 30 mg/g [vs 5 mg/g], 1·50; 1·35-1·65 vs 1·52; 1·38-1·67). The overall interactions were not significant. We identified much the same findings for ESRD in the chronic kidney disease cohorts. Despite higher risks for mortality and ESRD in diabetes, the relative risks of these outcomes by eGFR and ACR are much the same irrespective of the presence or absence of diabetes, emphasising the importance of kidney disease as a predictor of clinical outcomes. US National Kidney Foundation. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Mechanical factors in arterial aging: a clinical perspective.

            The human arterial system in youth is beautifully designed for its role of receiving spurts of blood from the left ventricle and distributing this as steady flow through peripheral capillaries. Central to such design is "tuning" of the heart to arterial tree; this minimizes aortic pressure fluctuations and confines flow pulsations to the larger arteries. With aging, repetitive pulsations (some 30 million/year) cause fatigue and fracture of elastin lamellae of central arteries, causing them to stiffen (and dilate), so that reflections return earlier to the heart; in consequence, aortic systolic pressure rises, diastolic pressure falls, and pulsations of flow extend further into smaller vessels of vasodilated organs (notably the brain and kidney). Stiffening leads to increased left ventricular (LV) load with hypertrophy, decreased capacity for myocardial perfusion, and increased stresses on small arterial vessels, particularly of brain and kidney. Clinical manifestations are a result of diastolic LV dysfunction with dyspnea, predisposition to angina, and heart failure, and small vessel degeneration in brain and kidney with intellectual deterioration and renal failure. While aortic stiffening is the principal cause of cardiovascular disease with age in persons who escape atherosclerotic complications, it is not a specific target for therapy. The principal target is the smooth muscle in distributing arteries, whose relaxation has little effect on peripheral resistance but causes substantial reduction in the magnitude of wave reflection. Such relaxation is achieved through regular exercise and with the vasodilating drugs that are used in modern treatment of hypertension and cardiac failure.
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              2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.


                Author and article information

                S. Karger AG
                May 2015
                27 February 2015
                : 2
                : 1-4
                : 81-94
                Department of Cardiology, Tokyo Medical University, Tokyo, Japan
                Author notes
                *Hirofumi Tomiyama, MD, Department of Cardiology, Tokyo Medical University, Nishi-Shinjuku, Tokyo 6-7-1 (Japan), E-Mail tomiyama@tokyo-med.ac.jp
                374092 PMC4646141 Pulse 2014;2:81-94
                © 2015 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 55, Pages: 14
                Arterial Stiffness and the Kidney


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