The first edition of Comorbidities in Chronic Kidney Disease is focused on the main clinical syndromes associated with renal failure. Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are characterized by a wide spectrum of comorbidities, potentially complicating patients clinical outcomes. In this volume, both editor and authors have planned a complete review of the main clinical syndromes associated with renal injury and failure. The first chapter is dedicated to epidemiological aspects of chronic kidney disease, and also introduces risk factors and associated comorbidities. Arterial hypertension and cardiovascular diseases are actually accountable as major risk factors for developing renal disease, and the next chapter is mainly focused on the latest trials in this field. The following chapter is dedicated to pathophysiology, diagnosis and treatment of dyslipidemia and atherosclerosis in patients with declined renal function. The subsequent chapter is exhaustively focused on the clinical features of secondary hyperparathyroidism and the diseases complications on kidneys, bone, vessels and heart, from early laboratory findings to severe vascular and heart valvular calcifications. The section that succeeds reflects on secondary anemia and consequent cardiorenal anemia syndrome with particular attention on the latest treatment schedules. Coronary artery disease is also discussed, especially for those concerned with clinical features and laboratory diagnosis in chronic kidney disease patients with impaired clearance of coronary acute syndrome biomarkers. Cardiorenal syndrome and sudden cardiac death are well-established clinical aspects in CKD patients, and they are discussed both in terms of pathophsysiological and clinical features. The book finally ends with two sections on hepato-renal syndrome and contrast-induced nephropathy (CIN). CIN represents daily challenges for all nephrologists because due to the large amounts of instrumental diagnostic tests and an increasing number of chronic kidney disease patients involved. This volume could be appreciated both by nephrologists and all clinicians involved in chronic patients management due to schematic and practical editing and form.

This book aims to present a comprehensive classification of hypertensive phenotypes based on underlying target organ involvement. Particular emphasis is placed on review and assessment of clinical presentation, pathophysiologic mechanisms, and possible specific therapeutic options for each hypertension phenotype. Several of these phenotypes are well known and well described in the literature, such as prehypertension, white coat and masked hypertension, isolated systolic hypertension, renovascular hypertension, endocrine hypertension, pediatric hypertension, and gestational hypertension. Other hypertension phenotypes, however, are not widely recognized, being reported only in special reviews; examples include hypertension associated with renal calculus disease and other rarer causes such as Turner syndrome, herbal and medicinal compounds, and pharmacologic agents. A detailed account of the various causes of monogenic hypertension is also included. Finally, a section is devoted to general aspects of hypertension, including the significance of blood pressure indices, the natural course of untreated and treated hypertension, hypertension mechanisms, genetics, and guidelines for blood pressure control.

Critical References Nephrology (Edition 1) contains the essential references for each of 62 topics in adult clinical nephrology. With each reference, the authors have explained how that research study contributed to the clinical topic of interest, providing immediate context. Critical References Nephrology (Edition 1) is an invaluable reference, serving as an easy guide for exam preparation, daily clinical practice and preparation of both research articles and teaching sessions. By summarizing the major findings of the most important research studies, Critical References Nephrology quickly provides the most evidence based information of all major nephrology topics.

This book reviews important aspects of polycystic kidney diseases, the latest scientific understanding of the diseases and syndromes, along with the therapies being developed. Cystic kidney diseases comprise a spectrum of genetic syndromes defined by renal cyst formation and expansion with variable extrarenal manifestations. The most prevalent disorder is the autosomal dominant polycystic kidney disease (ADPKD). It is the most common monogenetic disorder in humans and accounts for 4.4% of end-stage renal disease (ESRD) cases in the U.S. Patients inevitably progress to ESRD and require renal replacement therapy in the form of dialysis or transplantation. Through advancements in genomics and proteomics approaches, novel genes responsible for cystic diseases have been identified, further expanding our understanding of basic mechanisms of disease pathogenesis. The hallmark among all cystic genetic syndromes is the formation and growth of fluid-filled cysts, which originate from tubular epithelia of nephron segments. Cysts are the disease, and treatment strategies are being developed to target prevention or delay of cyst formation and expansion at an early stage, however no such therapy is currently approved.

Acute kidney injury (AKI) is a major health concern because it is associated with increased morbidity and mortality. While therapies for AKI have improved in recent years, the prevalence of this condition is still high and continues to increase. Considering these clinical issues, the appropriate detection and management of risk factors related to AKI are important issues for clinicians managing AKI patients. This book discusses the forms of detection, predictors and long-term outcomes for acute kidney injuries.

The two kidneys of mammalian organisms receive around 25 % of the cardiac output at rest, of which only 7 % is distributed to the renal medulla. Despite the low blood flow to the renal medulla, small changes in perfusion to the region can have profound effects on urine-concentrating ability and the excretion of sodium, which in turn affects the chronic regulation of body fluid volumes and arterial blood pressure. Importantly, we know that if blood flow to the renal medulla is not tightly regulated, sodium and water homeostasis is impaired and medullary hypoxia develops. The resultant injury inevitably reduces urine concentrating ability and leads to hypertension. This book will discuss the variety of mechanisms that mammalian organisms have developed to ensure that renal medullary blood flow and oxygen levels are precisely regulated. This book will focus on the unique anatomical arrangement of the medullary circulation, the functional roles of medullary blood flow, as well as the experimental techniques used to assess medullary blood flow and the insight that these studies have provided. The hormonal and non-hormonal control of medullary blood flow will be considered and finally the impact of reduced medullary blood flow on blood pressure is discussed.