Seminars in Nephrology RSS feed: Current Issue. Seminars in Nephrology is a timely source for the publication of new concepts and research findings relevant to clinical practice. Each issue is an organized compendium of practical information that serves as a lasting reference for nephrologists, internists and physicians in training. 2011 Topics , Volume 31, Issues 1-6 January Pregnancy and the Kidney S. Ananth Karumanchi and Marshall Lindheimer March Endothelium and the Kidney Philip Marsden May Peritoneal Dialysis Joanne Bargman July Imaging Techniques in Nephrology Bruce Molitoris September Uric Acid and the Kidney Richard Johnson November Glomerulonephritis Richard J. Glassock http://www.seminarsinnephrology.org/?rss=yesElsevier Inc.en © 2012 Published by Elsevier Inc. All rights reserved. Seminars in Nephrology0270-9295321January 2012 © 2012 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.seminarsinnephrology.org/article/PIIS0270929512000095/abstract?rss=yesMasthead10.1016/S0270-9295(12)00009-5Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0IFCIFChttp://www.seminarsinnephrology.org/article/PIIS027092951100180X/abstract?rss=yesHeart/kidney interactions and their clinical consequences have been a subject of debate for many years. Progress has been limited by a lack of a systematic approach to the subject as well as the organ-oriented rather than patient-oriented focus of specialists. Furthermore, current medical education centered on single specialties rather than a more holistic approach to the patient have held back progress in the comprehension of pathophysiological mechanisms and possible therapeutic strategies of heart/kidney combined disorders.Cardio-Renal Syndromes: IntroductionClaudio Ronco10.1016/j.semnephrol.2011.11.001Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-012http://www.seminarsinnephrology.org/article/PIIS0270929511001811/abstract?rss=yesSummary: Chronic heart failure and chronic renal failure are at epidemic proportions. These patients have significantly altered cardiac, renal, and all-cause outcomes. Much of the current research has focused on treating these individual organs in isolation. Although there are positive data on outcomes with neurohormonal modulation, they, however, remain underused. At present, data lacks for novel treatment options, while evidence continues to point at significantly worsened prognosis. Current diagnostic tools that detect acute changes in renal function or renal injury appear retrospective, which often hinder meaningful diagnostic and therapeutic decisions. This review is aimed at exploring the importance of accurate assessment of renal function for the heart failure patient by providing a synopsis on cardio-renal physiology and establishing the possibility of novel approaches in bridging the divide. Cardio-Renal Syndrome: New Perspective in DiagnosticsP. Iyngkaran, H. Schneider, P. Devarajan, N. Anavekar, H. Krum, C. Ronco10.1016/j.semnephrol.2011.11.002Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0317http://www.seminarsinnephrology.org/article/PIIS0270929511001823/abstract?rss=yesSummary: One third of heart failure admissions may be complicated by acute kidney injury, resulting in a three-fold increase in length of stay and a greater likelihood of rehospitalization. Cardio-Renal syndrome type 1 refers to acute decompensation of cardiac function leading to acute renal failure. It often complicates acute coronary syndrome and acute decompensated heart failure. Both components of the syndrome contribute to morbidity and mortality. The pathophysiology of renal dysfunction is complex. Reduced cardiac output, passive congestion of the kidneys, and increased intra-abdominal pressure may contribute to the disorder. The heart, kidneys, renin-angiotensin system, sympathetic nervous system, immune system, and vasculature interact through intricate feedback loops. An imbalance in this complex system often will cause deterioration in both cardiac and renal function. Appreciation of these interactions is crucial to understanding the overall burden of disease, as well as its natural history, risk factors, associated morbidity and mortality, and therapeutic implications. Cardio-Renal Syndrome Type 1: Epidemiology, Pathophysiology, and TreatmentYousif Ismail, Zaid Kasmikha, Henry L. Green, Peter A. McCullough10.1016/j.semnephrol.2011.11.003Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-01825http://www.seminarsinnephrology.org/article/PIIS0270929511001835/abstract?rss=yesSummary: Cardiac and kidney disease are becoming increasingly more prevalent in the population, and may exist concurrently. One of the most important comorbidities in heart failure is renal dysfunction. The pathophysiology of cardio-renal syndromes is complicated, and has been divided into five categories. Cardio-Renal syndrome type 2 is described by chronic cardiac abnormalities resulting in impaired renal function. It is important to recognize this entity and to understand the pathophysiology underlying the cardiac and renal disorders to distinguish best treatment practices. The success in improved outcomes lies in optimization of heart failure therapies. Cardio-Renal Syndrome Type 2: Epidemiology, Pathophysiology, and TreatmentPreeti Jois, Alexandre Mebazaa10.1016/j.semnephrol.2011.11.004Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-02630http://www.seminarsinnephrology.org/article/PIIS0270929511001847/abstract?rss=yesSummary: A complex pathophysiology, cardio-renal syndrome (CRS), has been redefined in recent years. One subtype is acute renocardiac CRS, or CRS type 3. This syndrome is intended to comprise situations in which acute kidney injury (AKI) results in acute cardiac injury or dysfunction. The pathophysiology of CRS type 3 is not well understood. Existing evidence suggests a bidirectional link between these two organ systems. The mechanisms whereby AKI leads to cardiac dysfunction have been proposed to include two categories: direct effects of AKI on the heart, and effects of AKI on remote organ function with indirect effects on the heart. AKI has been shown to cause inflammation in experimental renal ischemic models, which then induced cytokine expression, leukocyte infiltration into the heart, cell death by apoptosis, and impaired cardiac function. Combined with this finding is the well-known significant physiological derangements, such as fluid and electrolyte imbalance and uremia, that underpin remote organ failure and finally affect cardiac function, which in turn causes further kidney injury. This vicious cycle is fundamental to cardio-renal syndromes. The high morbidity and mortality is likely a result of this adverse synergy. A standard definition and diagnostic criteria are important first steps to approach this syndrome. Results obtained from studies using a standard definition of AKI can lead us to the next step of early recognition, prevention, therapeutic intervention, and improved quality of care. Novel biomarkers and therapeutic interventions for primary and secondary disorders are being developed and tested. The hope is that improved outcomes will follow. Cardio-Renal Syndrome Type 3: Epidemiology, Pathophysiology, and TreatmentAnan Chuasuwan, John A. Kellum10.1016/j.semnephrol.2011.11.005Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-03139http://www.seminarsinnephrology.org/article/PIIS0270929511001859/abstract?rss=yesSummary: Cardiovascular diseases such as coronary artery disease, congestive heart failure, arrhythmia, and sudden cardiac death represent the leading causes of morbidity and mortality in patients with CKD, increasing sharply as patients approach end-stage renal disease. The pathogenesis includes a complex, bidirectional interaction between the heart and kidneys that encompasses traditional and nontraditional risk factors, and has been termed cardio-renal syndrome type 4. In this review, an overview of the epidemiology and scope of this problem is provided, some suggested mechanisms for the pathophysiology of this disorder are discussed, and some of the key treatment strategies are described, with particular focus on recent clinical trials, both negative and positive. Cardio-Renal Syndrome Type 4: Epidemiology, Pathophysiology and TreatmentAndrew A. House10.1016/j.semnephrol.2011.11.006Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-04048http://www.seminarsinnephrology.org/article/PIIS0270929511001860/abstract?rss=yesSummary: The cardio-renal syndromes (CRS) recently were defined systematically as disorders of the heart or kidney whereby dysfunction of one organ leads to dysfunction of another. Five types of CRS are defined. The first four types describe acute or chronic cardio-renal or renocardiac syndromes. Type 5 CRS refers to secondary cardio-renal syndrome or cardio-renal involvement in systemic conditions. It is a clinical and pathophysiological entity to describe the concomitant presence of renal and cardiovascular dysfunction. Type 5 CRS can be acute or chronic and it does not strictly satisfy the definition of CRS. However, it encompasses many conditions in which combined heart and kidney dysfunction is observed. Because this entity has been described only recently there is limited information about the epidemiology, clinical course, and treatment of this condition. Cardio-Renal Syndrome Type 5: Epidemiology, Pathophysiology, and TreatmentSachin S. Soni, Claudio Ronco, Rupesh Pophale, Ashish S. Bhansali, Amit P. Nagarik, Shriganesh R. Barnela, Sonali S. Saboo, Anuradha Raman10.1016/j.semnephrol.2011.11.007Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-04956http://www.seminarsinnephrology.org/article/PIIS0270929511001872/abstract?rss=yesSummary: Chronic heart failure is a common disorder associated with unacceptably high mortality rates. Chronic renal disease and anemia are two important comorbidities that significantly influence morbidity and mortality in patients with chronic heart failure (CHF). Progress in CHF again may cause worsening of kidney function and anemia. To describe this vicious cycle, the term cardio-renal anemia syndrome has been suggested. Iron deficiency is part of the pathophysiology of anemia in both CHF and chronic kidney disease, which makes it an interesting target for treatment of anemia in cardio-renal anemia syndrome. Recently, studies have highlighted the potential clinical benefits of treating iron deficiency in patients with CHF, even if these patients are nonanemic. This article summarizes studies investigating the influence of iron deficiency with or without anemia in chronic kidney disease and CHF and gives an overview of preparations of intravenous iron currently available. Role of Iron Deficiency and Anemia in Cardio-Renal SyndromesPhilipp Attanasio, Claudio Ronco, Stefan D. Anker, Mariantonietta Cicoira, Stephan von Haehling10.1016/j.semnephrol.2011.11.008Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-05762http://www.seminarsinnephrology.org/article/PIIS0270929511001884/abstract?rss=yesSummary: The involvement of vitamin D deficiency in cardiovascular morbidity and mortality is attracting great interest. In patients with chronic kidney disease this association is stronger because vitamin D levels decrease as a result of renal progressive impairment. In chronic kidney disease secondary hyperparathyroidism commonly occurs in response to persistent hypocalcemia and hyperphosphatemia; moreover, parathyroid gland volume increases, vascular calcification is accelerated, and structural and functional modifications of the left ventricle are observed. These alterations entail both cardiac and renal involvement, resulting in cardio-renal syndrome. Recent studies concluded that vitamin D administration seems to have cardioprotective and renoprotective effects and improve peripheral vascular disease, vascular calcification, cardiac outcome, and blood pressure control. In clinical practice, therefore, the use of this hormone may play an important role in cardio-renal syndrome prevention. Role of Vitamin D Receptor Activators in Cardio-Renal SyndromesMario Cozzolino, Elena Bruschetta, Andrea Stucchi, Claudio Ronco, Daniele Cusi10.1016/j.semnephrol.2011.11.009Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-06369http://www.seminarsinnephrology.org/article/PIIS0270929511001896/abstract?rss=yesSummary: Cardiovascular and kidney diseases are highly prevalent and frequently are seen in the same patient. This overlap between cardiac and kidney diseases, in part, relates to common etiologies such as diabetes and hypertension. However, there are important dynamic and bidirectional interactions between the cardiovascular system and kidneys that may explain the occurrence of organ dysfunction. In this regard, it is clear that inflammation plays an important role in the pathogenesis of both cardiovascular and renal diseases. Given the circulating nature of many inflammatory mediators (cytokines, immune cells), it is tempting to speculate that the immune system can act as a mediator of organ cross-talk and may be involved in the reciprocal dysfunction that is encountered commonly in cardio-renal syndromes. The Role of Inflammation in the Cardio-Renal Syndrome: A Focus on Cytokines and Inflammatory MediatorsMitchell H. Rosner, Claudio Ronco, Mark D. Okusa10.1016/j.semnephrol.2011.11.010Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-07078http://www.seminarsinnephrology.org/article/PIIS0270929511001902/abstract?rss=yesSummary: The complex interaction between heart and kidney disease has been increasingly recognized over the recent years. Pathologies within these two organs frequently coexist and, due to organ cross-talk, dysfunction in one often leads to problems in the other. The classification of the various forms of cardio-renal syndrome has made these interactions clearer. To aid in the diagnosis, management and prognosis of these conditions, many novel cardiac and renal biomarkers have emerged to supplement traditional markers which have limited specificity and sensitivity. In this review we will summarize the literature on novel renal behind these and other biomarkers and discuss their potential relevance to the clinical scenarios of cardio-renal syndrome. Role of Biomarkers in the Diagnosis and Management of Cardio-Renal SyndromesDinna N. Cruz, Arrash Fard, Anna Clementi, Claudio Ronco, Alan Maisel10.1016/j.semnephrol.2011.11.011Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-07992http://www.seminarsinnephrology.org/article/PIIS0270929511001914/abstract?rss=yesSummary: The cardio-renal syndromes (CRS) are the result of complex bidirectional organ cross-talk between the heart and kidney, with tremendous overlap of diseases such as coronary heart disease, heart failure (HF), and renal dysfunction in the same patient. Volume overload plays an important role in the pathophysiology of CRS. The appropriate treatment of overhydration, particularly in HF and in chronic kidney disease, has been associated with improved outcomes and blood pressure control. Clinical examination alone is often insufficient for accurate assessment of volume status because significant volume overload can exist even in the absence of peripheral or pulmonary edema on physical examination or radiography. Bioelectrical impedance techniques increasingly are being used in the management of patients with HF and those on chronic dialysis. These methods provide more objective estimates of volume status in such patients. Used in conjunction with standard clinical assessment and biomarkers such as the natriuretic peptides, bioimpedance analysis may be useful in guiding pharmacologic and ultrafiltration therapies and subsequently restoring such patients to a euvolemic or optivolemic state. In this article, we review the use of these techniques in CRS. Role of Bioimpedance Vectorial Analysis in Cardio-Renal SyndromesNadia Aspromonte, Dinna N. Cruz, Claudio Ronco, Roberto Valle10.1016/j.semnephrol.2011.11.012Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-09399http://www.seminarsinnephrology.org/article/PIIS0270929511001926/abstract?rss=yesSummary: Acute decompensated heart failure and fluid overload are the most common causes of hospitalization in heart failure patients and they often contribute to disease progression. Initial treatment encompasses intravenous diuretics, although there might be a percentage of patients refractory to this pharmacologic approach. New technologies have been developed to perform extracorporeal ultrafiltration in fluid-overloaded patients. Newer simplified devices permit ultrafiltration to be performed with peripheral venous access and low blood flows, making ultrafiltration feasible at most hospitals and acute care settings. Extracorporeal ultrafiltration then is prescribed and conducted by specialized teams and fluid removal is planned to restore a status of hydration close to normal. Recent clinical trials, and European and North American practice guidelines, suggest that ultrafiltration is reasonable for patients with refractory congestion not responding to medical therapy and assigned to this recommendation a class IIa, level of evidence B. It seems that a close collaboration between nephrologists and cardiologists may be the key for a collaborative therapeutic effort in heart failure patients. Further studies suggest that wearable technologies might become available soon to treat patients in ambulatory and de-hospitalized settings. These new technologies may help to cope with the increasing demand for care of chronic heart failure patients. Extracorporeal Ultrafiltration in Heart Failure and Cardio-Renal SyndromesMaria Rosa Costanzo, Mario Cozzolino, Nadia Aspromonte, Flavio Mistrorigo, Roberto Valle, Claudio Ronco10.1016/j.semnephrol.2011.11.013Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0100111http://www.seminarsinnephrology.org/article/PIIS0270929511001938/abstract?rss=yesSummary: Heart failure is a syndrome in which myocardial function is incapable of providing for normal physiologic needs. In the acute care setting, cardiac dysfunction primarily manifests with volume perturbations and presents with signs and symptoms of vascular congestion. Thus, in acute heart failure volume assessment is crucial in diagnosing and improving the prognosis. Also, goal-directed therapy relies on accurate volume assessment to minimize the adverse outcomes of inappropriate, ineffective, or excessive diuresis. Currently, in most institutions clinical methods of volume assessment are the mainstay. However, these methods are highly dependent on the practitioners' skill level. In fact, there is a high variability between experienced physicians when assessing volume. As adjuncts, objective methods of volume assessment are being developed and used such as natriuretic peptides, bioimpedance analysis, and imaging. Fluid Overload Assessment and Management in Heart Failure PatientsTertius Tuy, W. Frank Peacock10.1016/j.semnephrol.2011.11.014Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0112120http://www.seminarsinnephrology.org/article/PIIS027092951100194X/abstract?rss=yesSummary: Cardio-Renal syndrome (CRS) is a common and complex clinical condition in which multiple causative factors are involved. The time window between renal insult and development of acute kidney injury (AKI) in acute heart failure (AHF) can be varied in different patients and AKI often is diagnosed too late, only when the effects of the insult become evident with a loss or decline of renal function. For this reason, pharmaceutical interventions for AKI that have been shown to be renoprotective or beneficial when tested in experimental conditions do not display similar results in the clinical setting. In most cases patients with AHF are admitted with clinical signs and symptoms of congestion and fluid overload. Loop diuretics, typically used to induce an enhanced diuresis in these congested patients, often are associated with a subsequent significant decrease in glomerular filtration rate and cause a creatinine increase that is apparent within 72 hours. Early detection of AKI is not possible with the use of serum creatinine and there is a need for a timely diagnostic tool able to address renal damage while it is happening. We need to define the diagnosis of both AHF and AKI in the early phases of CRS type 1 by coupling a kidney damage marker such as neutrophil gelatinase-associated lipocalin (NGAL) with B-type natriuretic peptide (BNP). Indeed, it would be ideal to make available a panel including whole blood or plasma cardiac and renal biomarkers building specific, pathophysiologically based, molecular profiles. Based on current knowledge and consensus, we can use kidney damage biomarkers such as plasma NGAL for an early diagnosis of AKI. However, differences in individual patient values and uncertainties about the ideal cut-off values may currently limit the application of these biomarkers. We propose that NGAL may increase its usefulness in the diagnosis and prevention of CRS if a curve of plasma values rather than a single plasma measurement is determined. To apply the concept of measuring an NGAL curve in AHF patients, however, assay performance in the lower-range values becomes a critical factor. For this reason, we propose the use of the new extended-range plasma NGAL assay that may contribute to remarkably improve the sensitivity of AKI diagnosis in AHF and lead to more effective intervention strategies. Neutrophil Gelatinase-Associated Lipocalin Curve and Neutrophil Gelatinase-Associated Lipocalin Extended-Range Assay: A New Biomarker Approach in the Early Diagnosis of Acute Kidney Injury and Cardio-Renal SyndromeClaudio Ronco, Dinna Cruz, Brian W. Noland10.1016/j.semnephrol.2011.11.015Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0121128http://www.seminarsinnephrology.org/article/PIIS0270929511001951/abstract?rss=yesSummary: Cardio-Renal syndrome may occur as a result of either primarily renal or cardiac dysfunction. This complex interaction requires a tailored approach to manage the underlying pathophysiology while optimizing the patient's symptoms and thus providing the best outcomes. Patients often are admitted to the hospital for signs and symptoms of congestion and fluid overload is the most frequent cause of subsequent re-admission. Fluid management is of paramount importance in the strategy of treatment for heart failure patients. Adequate fluid status should be obtained but a target value should be set according to objective indicators and biomarkers. Once the fluid excess is identified, a careful prescription of fluid removal by diuretics or extracorporeal therapies must be made. While delivering these therapies, adequate monitoring should be performed to prevent unwanted effects such as worsening of renal function or other complications. There is a very narrow window of optimal hydration for heart failure patients. Overhydration can result in myocardial stretching and potential decompensation. Inappropriate dehydration or relative reduction of circulating blood volume may result in distant organ damage caused by inadequate perfusion. We suggest consideration of the “5B” approach. This stands for balance of fluids (reflected by body weight), blood pressure, biomarkers, bioimpedance vector analysis, and blood volume. Addressing these parameters ensures that the most important issues affecting symptoms and outcomes are addressed. Furthermore, the patient is receiving the best possible care while avoiding unwanted side effects of the treatment. Diagnosis and Management of Fluid Overload in Heart Failure and Cardio-Renal Syndrome: The “5B” ApproachClaudio Ronco, Manish Kaushik, Roberto Valle, Nadia Aspromonte, W. Frank Peacock10.1016/j.semnephrol.2011.11.016Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0129141http://www.seminarsinnephrology.org/article/PIIS0270929512000113/abstract?rss=yesTable of Contents10.1016/S0270-9295(12)00011-3Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0FrontmatterA1A2http://www.seminarsinnephrology.org/article/PIIS0270929512000101/abstract?rss=yesEditorial Advisory Board10.1016/S0270-9295(12)00010-1Seminars in Nephrology 32, 1 (2012)2012-01-01Seminars in Nephrology2012-01-01321S0270-9295(12)X0002-0FrontmatterA3A3