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Atherosclerotic renal artery stenosis commonly co-exists with systolic and/or diastolic heart failure and is an unfavorable prognostic indicator. The morbidity and mortality relates to a complex neurohormonal interplay whereby renal ischemia activates the renin angiotensin aldosterone axis resulting in sodium retention, arterial vasoconstriction, and accelerated end-organ damage. In a subset of patients, particularly with bilateral renal artery stenosis, acute episodes of severe hypertension may lead to ˵flash″ pulmonary edema. Often sharing a common pathophysiology renal artery stenosis is especially common amongst heart failure patients with a 31 % incidence in those who undergo renal artery revascularization. The best course of treatment of renal artery stenosis in the setting of heart failure remains unclear. Although renal artery stenting has no effect on mortality, revascularization may lead to improved control of heart failure as evidenced by a reduction in hospital admissions and improvement in NYHA heart failure class. [ABSTRACT FROM AUTHOR]

Acute kidney injury remains a major clinical problem associated with poor patient outcome and therapeutic options are still limited. The transcription of hypoxia-inducible factors (HIF) is a key regulator of the cellular response to hypoxia. Far more than 100 HIF target genes have been identified, including genes that have been demonstrated to protect the kidney. Although renal cells have a broad capacity to activate HIF, HIF is only sporadically stabilized in cases of acute renal injury and therefore protective effects may be limited. Newly identified inhibitors of the oxygen-sensing HIF-prolyl-hydroxylases now offer the possibility to pharmacologically stabilize HIF independent of oxygen prior to a renal insult in order to achieve protection. Thus, HIF activation appears as a promising therapeutic target for the prevention of acute kidney injury. [ABSTRACT FROM AUTHOR]

In recent years the interference of heart and kidney disease has increasingly found attention in basic science and clinical research. A new classification of cardiorenal syndromes has now been proposed to address acute and chronic heart or kidney disease with its consequences on the respective other organ. However, it also becomes clear that the different clinical cardiorenal syndromes share common pathways. These basically include activation of the renin angiotensin system and of the sympathetic nervous system, but also inflammation, fibrosis, and accelerated atherosclerosis. These factors eventually support generation of oxidative stress and tissue hypoxia in the kidney and heart, culminating in irreversible tissue damage and aggravation of organ ischemia. This chapter summarizes aspects of the cardiorenal connection and oxygenation imbalances. [ABSTRACT FROM AUTHOR]

Many national registries and epidemiological observations have revealed a strong correlation between morbidity and mortality of patients with cardiovascular disease and kidney dysfunction. In patients with heart failure, renal dysfunction is highly prevalent. Even mild to moderate renal dysfunction in patients with congestive heart failure, i.e., cardiorenal syndrome, leads to significant increase in morbidity and mortality. The mechanisms underlying this complicated syndrome are not well elucidated, but the kidney is known to be responsible for the sodium and water retention in heart failure. Without better understanding the pathophysiology of this complex interaction between the heart and kidney, the outcome for these patients remains poor. Moreover, renal parenchymal disease is a pathogenic factor to cardiovascular disease independent of the role of traditional risk factors. More than 88% of patients with chronic kidney disease never reach end-stage renal disease, as the majority of them die due to cardiovascular disease. Thus, understanding the role of renal parenchymal disease as an independent cardiovascular risk state – i.e., renocardiac syndrome – is very important. In this chapter, we discuss the importance of renal function in the pathophysiology of congestive heart failure. We also elaborate on the novel understanding of chronic kidney disease and its role in cardiovascular disease progression. It should be stated that there may be involvement of both the cardiorenal and renocardiac syndromes associated with a systemic disease, such as with diabetes mellitus. [ABSTRACT FROM AUTHOR]

A strong relationship between chronic kidney disease (CKD) and accelerated cardiovascular disease, defined as the cardiorenal syndrome, is well documented, whether the initial event is in the kidney or in the heart. In the kidney context, mechanisms that link CKD and cardiovascular disease (CVD) involve both conventional and CKD (uremia)-related CVD risk factors. Several pathophysiologic processes responsible for the accelerated CVD spectrum in the CKD population include accelerated calcific occlusive atheromatous disease, diffuse nonocclusive medial-wall calcification, endothelial dysfunction, and uremic cardiomyopathy. In the heart context, disturbed CV dynamics and activation of neurohormonal and inflammatory factors are involved in the initiation of renal functional impairment and progressive kidney disease. The aim of this chapter is to present an overview of various aspects of cardiorenal association and to pinpoint features that are specific to each clinical entity, whether the initial insult is renal or cardiac. A detailed discussion of the various aspects of cardiorenal association are well covered in the following chapters. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a well established risk factor for cardiovascular diseases (CVD). In addition, a significant proportion of diabetic patients go on to develop nephropathy. Moreover, the presence of nephropathy further increases the risk of CVD in patients with all stages of diabetic nephropathy, including microalbuminuria, macroalbuminuria, and renal failure. The fibrogenic cytokine transforming growth factor beta (TGF-β) and the vascular endothelial growth factor (VEGF) are implicated in the development of cardinal features of diabetic nephropathy, namely, mesangial expansion and albuminuria, respectively. The pathogenesis of CVD in diabetes is multifactorial and can be affected by metabolic factors, such as oxidative stress, glycoxidation, procoagulant states, and inflammation. Furthermore, endothelial dysfunction may lead to simultaneous development and progression of renal and cardiac pathology in diabetes. The risk of microvascular complications can be reduced by intensive glycemic control, whereas cardiovascular benefit is less clear. Intensified intervention involving other vascular risk factors, such as hypertension and dyslipidemia, demonstrated benefits in terms of both macrovascular and microvascular complications. In addition, treatment with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists is associated with a significant reduction in the risk for renal disease progression in diabetes, which parallels the reduced cardiovascular risk. Moreover, changes in microalbuminuria translate into parallel changes in renal and cardiovascular risk. Nephropathy in diabetic patients is, therefore, important in determining the risk for and outcomes from CVD, the improved understanding of the pathogenesis of renal and vascular disease in diabetes, and as a crucial factor in planning a comprehensive treatment approach to reducing CVD morbidity and mortality in diabetic patients. [ABSTRACT FROM AUTHOR]

Heart and kidney dysfunction are often associated, the primary disorder of one of these two organs being the cause of secondary involvement of the other. These interactions represent the pathophysiological basis of cardiorenal syndrome. Renal dysfunction is very common in heart failure patients, with a highly variable prevalence according to the subgroup of patients considered. The complex pathophysiologic interactions between heart and kidney are far from being completely understood. Several ˵cardiorenal connectors,″ which represent the major players of the neurohumoral response in heart failure, have been identified. They act both through and independently from extracellular fluid volume control. Another mechanism, more recently taken into great consideration, is that of increased central venous pressure. Anemia, very frequent in both heart and renal failure, is most probably the third condition of this deadly syndrome, sometimes also called cardiorenal-anemia syndrome. In patients with heart failure, renal function has a powerful prognostic significance. This is true both in chronic heart failure over a long follow-up and in acutely decompensated heart failure for in-hospital mortality. In patients with advanced heart failure, baseline glomerular filtration rate has been reported to be even more powerful than left ventricular ejection fraction in predicting mortality. The prognostic meaning of worsening renal failure during hospitalization for acute decompensated heart failure is, on the contrary, less clear. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the leading cause of mortality in patients with end-stage renal disease. Combined cardiac and renal dysfunction amplifies disease progression in both organs and increases the incidence of morbidity and mortality it these patients. This clinical condition is defined as cardiorenal syndrome, which was recently classified into five subtypes defined according to pathophysiology, time frame, and nature of coexisting cardiac and renal dysfunction. Chronic kidney disease (CKD) is an independent risk factor for CVD on a scale similar to that of traditional risk factors. The sympathetic nervous system and the renin-angiotensin system, both of which can be activated in CKD patients, are two major cardiovascular connectors contributing to cardiac and renal functional derangement and structural damage of the cardiorenal syndrome and thus are significant contributors to the pathogenesis of CVD morbility and mortality. [ABSTRACT FROM AUTHOR]