Cardiorenal connection in chronic kidney disease
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Chronic kidney disease (CKD), as defined by reduced glomerular filtration rate (<60 ml/min/1.73 m2) and/or the presence of renal damage for >3 months, is a significant threat for public health in modern societies. Recent epidemiological studies have demonstrated that CKD is a significant risk for cardiovascular events independently of classical risk factors such as hypertension, dyslipidemia and diabetes. The mechanisms by which CKD increases the risk of cardiovascular events are currently under intensive investigation. Among various components of CKD, microalbuminuria is of particular interest, because it is a significant risk factor not only in diabetic and hypertensive subjects but also in the general population. Microalbuminuria is also closely associated with salt sensitivity of blood pressure, and the salt sensitivity is an independent risk factor for cardiovascular disease even in normotensive subjects. Several factors are likely to be involved in such associations, including the renin–angiotensin system (RAS), oxidative stress and inflammation. In addition, there may be more specific hemodynamic mechanisms in the kidney and other vital organs underlying these associations. This review describes ‘the strain vessel hypothesis’ as a possible mechanism for cerebrocardiorenal connections. In addition we discuss the significance of underlying diseases as cardiovascular risks of CKD as well as the role of RAS inhibition in the management of CKD patients.