Books: 'Kidney replacement therapy (KRT)'

1

V, Bonomini, and Università di Bologna, eds. Biotechnology in renal replacement therapy. Basel: Karger, 1989.

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2

P, Paganini Emil, ed. Acute continuous renal replacement therapy. Boston: M. Nijhoff, 1986.

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3

Controversies in acute kidney injury. Basel: Karger, 2011.

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4

Sara, Blakeley, ed. Renal failure and replacement therapies. London: Springer, 2008.

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5

Ronco, C., and Ding Xiaoqiang. Acute kidney injury. Basel: Karger, 2016.

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6

Claude, Jacobs, ed. Optimal treatment strategies in end-stage renal failure. Oxford: Oxford University Press, 2002.

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7

International, Course on Critical Care Nephrology (3rd 2004 Vicenza Italy). Sepsis, kidney and multiple organ dysfunction: Proceedings of the Third International Course on Critical Care Nephrology, Vicenza, June 1-4, 2004. Basel: Karger, 2004.

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8

Marshall, Mark R. Intermittent acute renal replacement therapy. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0233_update_001.

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This chapter summarizes current best practice with respect to intermittent haemodialysis and sustained low-efficiency dialysis (SLED) for those with acute kidney injury. These modalities can be delivered using a variety of technology platforms. These platforms for the most part use online dialysate, and water quality needs to be monitored and maintained to current standards. Intermittent haemodialysis and SLED provide reasonable outcomes in experienced hands, and ameliorate morbidity and mortality resulting from the ‘acute uraemic syndrome’: that is, intractable infection, non-resolving shock, and haemorrhage.Careful consideration needs to be given to appropriate modality selection for patients. Lower-efficiency modalities such as continuous therapies or SLED are more appropriate for patients at risk from dialysis disequilibrium syndrome, those with abdominal compartment syndrome, and those who are haemodynamically unstable (including cardiogenic shock). Care should be taken to avoid complications related to rapid fluid and solute removal, anticoagulation, and vascular access. Intradialytic hypotension is detrimental for both general and renal recovery of critically ill patients, and can be mitigated by sodium and ultrafiltration profiling, and frequent treatments and prolonged treatment time to minimize ultrafiltration goals and rates.Irrespective of the modality applied, an adequate dialysis dose must be achieved. This is facilitated through the use of optimally placed and technically superior central venous catheters, and well-considered prescription of haemodialysis and SLED operating parameters. Dose should be monitored regularly through urea kinetic modelling, either using Kt/V for thrice-weekly schedules or the corrected equivalent renal urea clearance (EKRc) for more frequent ones.

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9

Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.

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Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.

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10

Ronco, Claudio, Rinaldo Bellomo, and John A. Kellum. Continuous Renal Replacement Therapy. Oxford University Press, Incorporated, 2016.

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11

A, Kellum John, Bellomo R. 1956-, and Ronco C. 1951-, eds. Continuous renal replacement therapy. Oxford: Oxford University Press, 2009.

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12

Kellum, John A. Continuous Renal Replacement Therapy. Oxford University Press, 2009.

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13

Acute Continuous Renal Replacement Therapy. Springer, 2012.

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14

Paganini, Emil P. Acute Continuous Renal Replacement Therapy. Springer London, Limited, 2012.

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15

Kidney Diseases And Renal Replacement Therapies. W.B. Saunders Company, 2011.

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16

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Renal replacement therapy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0168.

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Renal replacement therapies provide a substitute for the function of normal kidneys. Options include haemofiltration, haemodialysis, peritoneal dialysis, and renal transplantation. Haemofiltration is only used in the acute setting. Endocrine functions of the kidney are replaced with erythropoietin and vitamin D therapy. This chapter provides an overview of renal replacement therapies.

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17

Koch, Karl-Martin, Walter H. Hörl, J. F. Winchester, C. Ronco, and Robert M. Lindsay. Replacement of Renal Function by Dialysis. Springer London, Limited, 2004.

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18

Koch, Karl-Martin, Walter H. Hörl, C. Ronco, J. F. Winchester, and Robert M. Lindsay. Replacement of Renal Function by Dialysis. Springer, 2014.

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19

(Editor), Walter H. Hörl, K. M. Koch (Editor), Robert M. Lindsay (Editor), C. Ronco (Editor), and J. F. Winchester (Editor), eds. Replacement of Renal Function by Dialysis. 5th ed. Springer, 2004.

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20

H, Hörl Walter, ed. Replacement of renal function by dialysis. 5th ed. Dordrecht: Kluwer Academic Publishers, 2003.

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21

Won Seo, Jang, and Ravindra L. Mehta. Renal replacement therapy in the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0232_update_001.

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Several techniques for renal replacement therapy are now utilized to manage patients with acute kidney injury including intermittent haemodialysis, continuous renal replacement therapy, sustained low-efficiency dialysis, and peritoneal dialysis. This chapter provides an update on contemporary issues including advances in dialysis technology and its effects on the application of dialysis in acute kidney injury. The timing of initiation, modality choice, optimal dose, and management of complications in dialysis are some of the areas where there is controversy.

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22

1938-1984, Kramer Peter, ed. Arteriovenous hemofiltration: A kidney replacement therapy for intensive care unit. Berlin: Springer-Verlag, 1985.

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23

English, Arterio-Venous Hamofiltration. Arteriovenous Hemofiltration: A Kidney Replacement Therapy for the Intensive Care Unit. Springer, 1986.

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24

Kramer, Peter, and Gertrud Elisabeth Holle. Arteriovenous Hemofiltration: A Kidney Replacement Therapy for the Intensive Care Unit. Springer, 1985.

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25

Kramer, Peter. Arteriovenous Hemofiltration: A Kidney Replacement Therapy for the Intensive Care Unit. Springer London, Limited, 2012.

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26

Thuraisingham, Raj, and Cormac Breen. Modality selection for renal replacement therapy. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0141.

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The choice of treatment for end-stage kidney disease is an important one for patients. Ideally this should happen as a coordinated process over a period of time, supported by education and individualized treatment planning discussions to assist the patient in making an informed choice about their treatment. In this setting, patients suitable for transplantation may select this treatment modality and potentially, especially if there is a living kidney donor, be transplanted before the need for dialysis. Other patients may choose between dialysis modalities, between home and in-centre treatment, or in some cases between active dialysis treatment and conservative kidney care. A smaller proportion of patients may present with the urgent need to start dialysis, the crash-lander pathway. In this situation initial treatment planning and choice is more limited, treatment is more often determined by institutional practice, and treatment choice and formation of definitive dialysis access are achieved at a later date.

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27

Wong, Muh Geot, Bruce A. Cooper, and Carol A. Pollock. Preparation for renal replacement therapy. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0143_update_001.

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Although the primary aim of management in chronic kidney disease (CKD) is to prevent progression to stage 5 CKD, for many patients renal replacement therapy (RRT) is inevitable. Planning for the initiation of dialysis is aimed at ensuring that it takes place in a supported environment in which adverse events will be minimized, that the modality chosen is appropriate for the individual circumstances, and the patient has full knowledge of what RRT entails. Beginning dialysis inevitably involves medical, psychological, family, and social issues, and preparation for RRT is optimally managed by a team with appropriate expertise in these areas. Multidisciplinary education programmes that inform patients and their families about their disease and the treatment options are likely to result in patients starting dialysis in a planned and elective manner.

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28

Acute kidney injury. Basel: Karger, 2007.

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29

Schneider, Antoine G., Neil J. Glassford, and Rinaldo Bellomo. Choice of Renal Replacement Therapy and Renal Recovery. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0038.

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Acute kidney injury (AKI) is a major complication of critical illness, associated with increased mortality and morbidity. Among survivors of AKI, a subset will develop the need for chronic dialysis. Chronic dialysis imposes a major physical, emotional, economic, and social burden on ICU survivors and their caregivers. Evidence suggests that the type of renal replacement therapy used in the acute setting may affect renal recovery differently. For example, intermittent haemodialysis (IHD) increases the risk of hypotension and acute volume and solute fluctuations, and such physiological events have been associated with fresh renal injury. In contrast, continuous renal replacement therapy (CRRT) does not carry such risks. Consistent with such physiological and experimental observations and differences, several observational studies and some randomized controlled trials suggest that using IHD, instead of CRRT, as the preferred form of RRT increases the risk of patients entering a chronic dialysis programme. A recent meta-analysis confirmed these findings. Clinicians making decisions about the choice of RRT modality in ICU patients should carefully consider these observations.

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30

Vishnu, Moorthy A., ed. Pathophysiology of kidney disease and hypertension. Philadelphia, PA: Saunders/Elsevier, 2009.

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31

Acute Kidney Injury (Contributions to Nephrology). S. Karger AG (Switzerland), 2007.

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32

Ronco, Claudio, and Zaccaria Ricci. Renal support therapy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0029.

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Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.

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33

Ronco, Claudio, and Zaccaria Ricci. Renal support therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0029_update_001.

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Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.

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34

Ronco, Claudio, and Zaccaria Ricci. Renal support therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0029_update_002.

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Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.

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35

Sepsis, Kidney and Multiple Organ Dysfunction. Muenchen: Karger, 2005.

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36

Thomas, Nicola. Advanced Renal Care. Wiley & Sons, Incorporated, John, 2008.

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37

Thomas, Nicola. Advanced Renal Care. Wiley & Sons, Incorporated, John, 2008.

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38

Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.

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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.

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39

Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.

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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.

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40

Prout, Jeremy, Tanya Jones, and Daniel Martin. Kidney and body fluids. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0003.

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The physiology of body fluid compartments is revised in association with clinical assessment of fluid balance and the management of fluid-related abnormalities. Electrolyte and acid-base disorders; causes, consequences and management are summarized. Acute kidney injury in the context of perioperative medicine is discussed; including definitions, risks, causes, recognition, prevention and preventative measures. Renal replacement therapy strategies are explained.

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41

Pleniceanu, Oren, and Benjamin Dekel. Kidney stem cells. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0344.

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End-stage renal failure is a major cause of death with currently only dialysis and transplantation available as therapeutic options, each with its own limitations and drawbacks. To allow regenerative medicine-based kidney replacement therapies and due to the fact that neither haematopoietic stem cells nor mesenchymal stem cells, the most accessible human stem cells, can be used to derive genuine nephron progenitors, much attention has been given to finding adult renal stem cells. Several candidates for this have been described, but their true identity as stem or progenitor cells and their potential use in therapy has not yet been shown. However, the analysis of embryonic renal stem cells, specifically stem/progenitor cells that are induced into the nephrogenic pathway to form nephrons until the 34th week of gestation, has been much more conclusive.

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42

Bello, Aminu, Marcello Tonelli, and Kitty Jager. Epidemiology of kidney disease. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0001.

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Renal epidemiology has moved from a focus on patients treated with renal replacement therapy using data from renal registries, to a much broader view of acute and chronic kidney disease. A review of essential epidemiological concepts and principles is followed by discussion of the epidemiology of different types of kidney disease: acute kidney injury, chronic kidney disease, and end-stage renal disease. The chapter concludes with a section on future challenges and potential solutions.

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43

Fichtner, Alexander, and Franz Schaefer. Acute kidney injury in children. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0239.

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In the past few decades, the overall incidence of acute kidney injury (AKI) in paediatric patients has increased and the aetiological spectrum has shifted from infection-related and intrinsic renal causes towards secondary forms of AKI related to exposure to nephrotoxic drugs and complex surgical, oncological, and intensive care manoeuvres. In addition, neonatal kidney impairment and haemolytic uraemic syndrome continue to be important specific paediatric causes of AKI raising unique challenges regarding prevention, diagnosis, and treatment. The search for new biomarkers is a current focus of research in paediatric as in adult AKI research.Pharmacological intervention studies to prevent or attenuate AKI have provided positive evidence only for the prophylactic use of theophylline in severely depressed neonates, whereas dopamine and loop diuretics did not demonstrate any efficacy. Preliminary findings support a dose-dependent renoprotective action of fenoldopam in infants undergoing cardiac surgery.Critical issues in the management of AKI in children include fluid handling, maintenance of adequate nutrition, and the choice of renal replacement therapy modality. Observational studies have suggested an adverse impact of fluid overload and late start of renal replacement therapy, and a randomized clinical trial revealed detrimental effects of aggressive fluid bolus therapy in volume-depleted children.Technological advances have made it possible to apply continuous replacement therapies in children of all ages, including preterm neonates, using appropriately sized catheters, filters, tubing, and flow settings adapted to paediatric needs. However, the majority of children with AKI worldwide are still treated with peritoneal dialysis, and comparative studies demonstrating superiority of extracorporeal techniques over peritoneal dialysis are lacking.The outcomes of paediatric AKI are comparable to adult patients. In critically ill children, mortality risk increases with each stage of AKI; mortality rates typically range between 15% and 30% for all AKI stages and 30% to 60% in children requiring renal replacement therapy. Chronic kidney disease develops in approximately 10% of children surviving AKI.

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44

Jörres, Achim, Dietrich Hasper, and Michael Oppert. Coagulation disturbances in acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0231.

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Patients with acute kidney injury may suffer from disturbances of the coagulation systems, either as a consequence of uraemia, or on the basis of an underlying disease, or due to blood–membrane interaction and/or anticoagulation during renal replacement therapy. The implications of this for their management, and anticoagulation during renal replacement therapy, are discussed. Some specific circumstances, including thrombotic microangiopathy, are mentioned.

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45

Thomas, Nicola. Advanced Renal Care. Wiley & Sons, Limited, John, 2008.

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46

(Contributor), Cordelia Ashwanden, Jane Bentley (Contributor), Celia Eggeling (Contributor), and Nicola Thomas (Editor), eds. Advanced Renal Care. 2nd ed. Blackwell Publishing Limited, 2004.

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47

Ong, Albert C. M., and Richard Sandford. Autosomal dominant polycystic kidney disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0306_update_001.

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Based on an estimated population prevalence of between 1 in 400 and 1 in 1000, there are over 60,000 individuals with or at risk of developing complications associated with autosomal dominant polycystic kidney disease (ADPKD) in the United Kingdom. This equates to over 300,000 people in the United States and 7 million worldwide. Once diagnosed, an individual with ADPKD will require long-term medical follow-up and treatment with an unknown cost to national health care systems. A major proportion, probably two-thirds, will develop end-stage renal disease (ESRD) requiring renal replacement therapy—dialysis or transplantation. ADPKD is therefore the commonest genetic cause of ESRD. Most centres worldwide report that approximately one in ten patients receiving dialysis therapy have a diagnosis of ADPKD. Improvements in healthcare for individuals with ADPKD will therefore impact directly on patients, their families, and healthcare resources.

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48

Haynes, Richard J., and James A. Gilbert. Chronic kidney disease and dialysis. Edited by Rutger Ploeg. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0128.

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Chronic kidney disease (CKD) is a common disorder as currently defined. Patients with CKD face two major hazards: cardiovascular disease and—in a minority—progression to end-stage renal disease (ESRD). Advanced CKD also causes numerous metabolic and other complications. The management of CKD involves excluding acute kidney injury, diagnosing the cause of CKD, slowing progression, and detecting and treating complications. If patients do reach ESRD, then renal replacement therapy (RRT) options must be considered. These include haemodialysis, peritoneal dialysis, or transplantation. Haemodialysis requires creation of an arteriovenous fistula or insertion of a prosthetic graft while peritoneal dialysis necessitates the insertion of a catheter into the abdominal cavity. All forms of dialysis access are associated with complications both in the short and long term. However, they remain vital and central to the life and the well-being of the end-stage renal patient on dialysis.

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49

(Editor), C. Ronco, R. Bellomo (Editor), and G. LA Greca (Editor), eds. Blood Purification in Intensive Care: 2nd International Course on Critical Care Nephrology, Vicenza, May 2001: Proceedings (Contributions to Nephrology). S. Karger Publishers (USA), 2001.

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50

Morris, Peter J., and Jeremy R. Chapman. The evolution of kidney transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0275.

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The history of kidney transplantation starts in 1902 with Ullman transplanting kidneys between dogs, and Carrel’s development of vascular anastomotic techniques. The developments in the 1950s in Boston, Paris, and the laboratories of Medawar and others demonstrated both proof of the principle and some of the barriers to clinical kidney transplantation. The 1960s laid the groundwork for organ preservation, immunosuppression, and histocompatibility leading to the creation of transplant units in many countries. In the 1970s, there was steady progress in understanding the immunology of allograft rejection and its suppression. The advent of azathioprine used with steroids in the early 1960s resulted in 1-year graft survival rates of around 60% and patient survival of 90% in good units. However, with the introduction of ciclosporin in the early 1980s, renal transplantation became an even more reliable renal replacement option as there was a dramatic reduction in the incidence of irreversible acute rejection. The 1990s saw the introduction of both better immunosuppression and better infection prophylaxis, which further improved patient outcomes. The first decade of the twenty-first century has been characterized by the promise of new technologies in many areas, only some of which have delivered clinical benefit. Molecular human leucocyte antigen (HLA) typing and detection of antibodies to HLA antigens, standardized immunosuppression and anti-infective prophylaxis, surveillance biopsy, and developing systems for increasing donation rates are delivering major benefits. Gene biomarkers, stem cell therapy, and tolerance protocols have yet to make an impact. This chapter describes the historical development of transplantation and how it has yielded the results delivered in clinical practice today.

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Books on the topic 'Kidney replacement therapy (KRT)'

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