Книги: "End Stage Kidney Disease (ESKD)"

1

Friedman, Eli A. Present and future therapies for end-stage renal disease. New Jersey: World Scientific, 2010.

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2

Jassal, Sarbjit Vanita. Kidney transplantation in elderly patients with end-stage renal disease. Ottawa: National Library of Canada, 1998.

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3

United States. Agency for Health Care and Policy Research. Laboratory tests in end-stage renal disease patients undergoing dialysis. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.

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4

Green, Ira. Laboratory tests in end-stage renal disease patients undergoing dialysis. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.

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5

Green, Ira. Laboratory tests in end-stage renal disease patients undergoing dialysis. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.

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6

Green, Ira. Laboratory tests in end-stage renal disease patients undergoing dialysis. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.

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7

Green, Ira. Laboratory tests in end-stage renal disease patients undergoing dialysis. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1994.

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8

Florida. Legislature. House of Representatives. Committee on Health Regulation. Overview of kidney dialysis studies and providers of end stage renal disease care. [Tallahassee, Fla.]: The Committee, 2001.

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9

Halper, Thomas. The misfortunes of others: End-stage renal disease in the United Kingdom. Cambridge: Cambridge University Press, 1989.

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10

1938-, Hardy Mark A., ed. Psychosocial aspects of end-stage renal disease: Issues of our times. New York: Haworth Press, 1991.

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11

V, Wizemann, Kramer W, and Schütterle G, eds. The heart in end-stage renal failure: Etiology, symptoms, and management of uremic heart disease. Basel: Karger, 1986.

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12

Dimosthenis, Stamopoulos, ed. Magnetically assisted hemodialysis: A new strategy for the treatment of end stage renal disease. New York: Nova Science Publishers, 2008.

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13

A, Rettig Richard, and Levinsky Norman G. 1929-, eds. Kidney failure and the federal government. Washington, D.C: National Academy Press, 1991.

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14

G, Oreopoulos D., and International Symposium on Geriatric Nephrology, eds. Geriatric nephrology: The medical, psychosocial, nursing, financial, and ethical issues of treating end-stage renal disease in the elderly. Dordrecht: Nijhoff, 1986.

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15

United States. Congress. House. Committee on Ways and Means. Subcommittee on Health. Medicare End-Stage Renal Disease (kidney failure) Program: Hearing before the Subcommittee on Health of the Committee on Ways and Means, House of Representatives, One Hundred Fourth Congress, first session, April 3, 1995. Washington: U.S. G.P.O., 1996.

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16

Murtagh, Fliss E. M. End-stage kidney disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0156.

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End-stage kidney disease (ESKD) accounts for 1-2% of all deaths. Ageing populations means that this proportion will grow steadily over the coming years. Symptom burden in ESKD exceeds advanced cancer, with added renal-specific symptoms, such as itch and restless legs. Pain and depression are also more prevalent. Many renal symptoms go under-recognized and under-treated, especially as they arise from co-morbid conditions, rather than the renal disease itself. The most useful intervention to address symptoms is regular assessment of symptoms, using a valid and reliable global symptom score. Pharmacological interventions to alleviate symptoms need to take account of the severe constraints on using renally cleared drugs, and the high risk of toxicity from accumulation of parent compound or metabolites. The population with ESKD has extensive palliative care needs, and need significant medical, nursing, psychological, and social care to address these as their illness advances towards the end of life.

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17

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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18

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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19

Kinsella, Sinead, and John Holian. The effect of chronic renal failure on critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0218.

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The incidence of chronic kidney disease (CKD) and end-stage kidney disease (ESKD) is increasing, reflecting an increase in the incidence and prevalence of hypertension and type 2 diabetes. Patients with CKD and ESKD frequently experience episodes of critical illness and require treatment in an intensive care unit (ICU)setting. Management requires specific consideration of their renal disease status together with their acute illness. Mortality in critically-ill patients with ESKD is frequently related to their co-morbid conditions, rather than their ESKD status. Illness severity scoring systems allocate high points for renal variables and tend to overestimate actual mortality. Patients with ESKD and CKD requiring ICU admission have better ICU and in-hospital survival than patients with denovo acute kidney injury requiring renal replacement therapy. Appropriately selected patients benefit from ICU admission and full consideration for ICU care should be given to these patients if required, despite their renal disease status. Cardiovascular disease and sepsis account for the majority of ICU admissions in this population and the aetiology of these conditions differs from that in patients without kidney disease. Optimal critical care management of patients with ESKD and CKD requires that these differences are recognized.

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20

Ong, Albert C. M., and Timothy Ellam. Autosomal dominant polycystic kidney disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0307_update_001.

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Autosomal dominant polycystic kidney disease (ADPKD) is responsible for up to 10% of prevalent patients with end-stage renal disease (ESRD). It is characterized by the enlargement of multiple bilateral renal cysts, present in almost all patients by their fifth decade. Loin pain is a common symptom that may be caused by cyst growth, intracyst haemorrhage, nephrolithiasis, or infection. Gross haematuria is also a common feature, but usually settles spontaneously. Excretory impairment develops after extensive cystic change has occurred and progresses to ESRD in half of all affected patients by the age of 60. However, the onset of cystic change and rate of renal functional decline are highly variable between individuals. ADPKD associated with the PKD1 gene has an earlier average age of cyst development and ESRD than PKD2, but the two cannot be distinguished on clinical grounds. Polycystins 1 and 2 are expressed in various organs and extrarenal disease may be the presenting feature. Intracranial aneurysms are five times more common in patients with ADPKD, but rupture is infrequent. Liver cysts are present in most patients and may be complicated by haemorrhage or infection, though liver failure is very rare. Massive hepatic cystic disease is confined to women, reflecting stimulatory effects of oestrogen on hepatic cyst growth. Cardiovascular disease is the leading cause of death in ADPKD and vascular dysfunction is present in many patients even before the development of excretory impairment. However, despite the multisystem manifestations of ADPKD, survival from ESRD is better for patients with ADPKD than for other non-diabetic causes of kidney failure.

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21

Ather, Sameer, Ayman Farag, Vikas Bhatia, and Fadi G. Hage. Role of Imaging in Chronic Kidney Disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0017.

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Cardiovascular disease is highly prevalent in patients with chronic kidney disease (CKD) and is the biggest contributor of death in these patients. Myocardial perfusion imaging (MPI) is a validated tool for diagnosing coronary artery disease (CAD) and for predicting short and long term prognosis in this patient population. Non-invasive stress imaging, with MPI or other imaging modalities, is widely used for risk stratification in patients with end-stage renal disease (ESRD) being evaluated for kidney transplantation due to the paucity of donor organs and the high cardiovascular risk of patients on the transplant waiting list. In this Chapter we will review the data on diagnostic accuracy and risk stratification using MPI in patients with CKD and ESRD highlighting the special challenges that are unique to this population. We will also discuss novel indicators that have been used in these patients to improve risk stratification.

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22

Hajhosseiny, Reza, Kaivan Khavandi, and David J. Goldsmith. Sudden cardiac death in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0108.

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Epidemiological data demonstrate the unique vulnerability of chronic kidney disease (CKD) subjects to cardiovascular disease, the most catastrophic being sudden cardiac death (SCD). In patients with declining kidney function there is a continuum of cardiovascular risk. In those individuals who survive to reach end-stage renal disease (ESRD), the risk of suffering a cardiac event is extremely high. Some of this risk is explained by the common risk factors and traditional cardiovascular events, namely atherosclerotic plaque fissure and rupture, but there is now evidence of a distinct ‘later CKD’ mechanism, notably arrhythmias. This appears particularly true in later stages of CKD and corresponds with the multifaceted range of myocardial and vascular insults operating. The physiological milieu of disordered vessel autoregulation, sequestered vasoprotective agents, loss of conduit and small artery elasticity/compliance, a stiffened and fibrotic myocardium, with calcified and diseased coronary arteries, all within an inflammatory environment, all contribute to arrhythmia generation. The final insult is changes in volume and electrolyte status. Risk stratification tools would be helpful in guiding clinicians to recognize those subjects likely to benefit from specific interventional strategies. These might include the novel, or emerging serum, haemodynamic, or electrocardiographic biomarkers in CKD. Current tools—such as those used for stratifying risk for SCD and determining the need for ICD implantation—are not valid in ESRD patients. Beta blockers appear likely to be generally advisable, blood pressure permitting, for patients with significant cardiomyopathy. Evidence for implantable cardiac defibrillators (ICD) is lacking. There is good reason to think that young dialysis patients at high risk of sudden death may benefit, but the risk/benefit ratio for older patients is less likely to be advantageous. These hypotheses need further investigation.

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23

Aina, Titilopemi A. O., and Miguel Prada. Kidney Transplantation. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0024.

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Patients with end-stage renal disease (ESRD) can be managed with kidney transplantation, hemodialysis, or peritoneal dialysis. The most common organ transplanted in the United States is the kidney. Kidney transplantation surgery can be divided into the following stages: incision/dissection of vessels, cross-clamping vessels, vascular anastomosis, unclamping of vessels, ureter anastomosis to bladder, and closing. The size of recipient and donor kidneys as well as the size of recipient blood vessels will determine the position of graft implantation—either intraperitoneal or extraperitoneal. At the conclusion of surgery, most of the patients are extubated. This chapter describes the key steps in the preoperative assessment, explains the features of intraoperative anesthetic management, reviews the risk factors for reintubation, and identifies the optimal plan for postoperative pain management.

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24

Lameire, Norbert. Renal outcomes of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0238_update_001.

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This chapter summarizes the accumulating evidence that incomplete or even apparent complete recovery of renal function after acute kidney injury (AKI) may be an important contributor to a growing number of incident chronic kidney disease (CKD) and end-stage renal disease (ESRD) cases, largely in excess of the global growth in CKD prevalence. Evidence based on epidemiologic studies supports the notion that even after adjustment for several important covariates AKI is independently associated with an increased risk for both CKD and ESRD. Several risk factors for the subsequent development of CKD among survivors of AKI have been identified. Besides well-known risk factors for CKD in general, such as hypertension, older age, congestive heart failure, diabetes, and proteinuria, AKIN staging and duration also predict longitudinal CKD development. These characteristics may identify a category of at-risk AKI patients at the time of hospital discharge that will need long follow-up times for appropriate screening and surveillance measures for CKD.

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25

Hundert, Joshua S., Rashmi Verma, Ritika Suri, Anika T. Singh, and Ajay Singh. Neurological Manifestations of Renal Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0191.

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In the United Syates, chronic kidney disease (CKD) affects approximately 5% to 10% of the general population. It is estimated that about 20 million Americans have some degree of CKD. Central nervous system (CNS) abnormalities are common in patients with CKD, especially in those individuals with end stage renal disease (ESRD) who require renal replacement therapy, such as dialysis or transplant. Neurological symptoms in patients with CKD may range from mild altered sensorium and cognitive dysfunction to tremors and coma. By the time patients require renal replacement therapy, some patients may have uremia, a clinical syndrome with protean manifestations.

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26

Naicker, Saraladevi, and Graham Paget. HIV and renal disease. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0187_update_001.

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The human immunodeficiency virus (HIV) infection epidemic has particularly affected the poorest regions of the world. HIV can directly or indirectly affect different aspects of renal function, and results in a variable expression of kidney disease.Acute kidney injury (AKI) occurs in approximately 20% of hospitalized patients. The prevalence of chronic kidney disease (CKD) amongst HIV-infected patients is reported at 3.5–38% in different regions of the world. The complex interplay between the pheno- and/or genotypic variants of the virus, the genetic make-up of the host, and environmental factors determine the clinical manifestations of renal disease. The association of APOL1 gene variants G1 and G2 with the risk of focal segmental glomerulosclerosis explains the high frequency of HIV-associated nephropathy (HIVAN) in populations of black ethnicity.Anti-retroviral therapy (ART) is effective in preventing progression of HIVAN. Some of the drugs used in ART regimens are potentially nephrotoxic and require dose adjustment or even avoidance in CKD. Progression to end-stage renal disease (ESRD) in HIVAN has been reported to correlate with the extent of chronic damage quantified by renal biopsy.HIV-infected patients requiring dialysis, who are stable on ART, are achieving survival rates comparable to those of non-HIV dialysis populations. Similarly, HIV infection does not seem to adversely affect patient and graft survival rates after kidney transplantation, and there has been no increase in the prevalence of opportunistic infections in transplant recipients on effective ART.

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27

Chenault, Kristin. Pediatric Renal Transplantation. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0043.

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Approximately 700 pediatric kidney transplants were performed in 2014, with roughly one-third of those being living-related kidney transplantations. There are distinct differences between renal disease and transplantation in children compared to adults. Overall, end-stage renal disease (ESRD) is less common in the pediatric population than in adults. While the most common etiology for ESRD in adults is diabetes mellitus, the most common etiologies of ESRD in the pediatric population are congenital, such as dysplastic kidney or obstructive uropathy. Surgical technique can also vary depending on the age and size of the recipient, as well as the donor kidney size.

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28

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

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29

Nissenson, Allen R., John Moran, and Robert Provenzano. Overview of dialysis patient management and future directions. Edited by Jonathan Himmelfarb. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0267_update_001.

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Nearly 2 million patients worldwide have end-stage renal disease (ESRD) and require dialysis or kidney transplantation. The advent of clinical dialysis in the 1950s has had a huge impact on the way ESRD and acute kidney injury are managed, but several decades later, the morbidity and mortality in patients with ESRD remain unacceptably high and patients often have a poor quality of life. Many believe that we have focused attention on a few key treatment-related outcomes, and have done well with these (i.e. anaemia, adequacy of dialysis, metabolic bone disease), but achieving great results in only these domains has clearly not been sufficient to drive improvements in survival or patient-reported outcomes. Recent experience with integrated care management, focusing on comorbidity management, offers promise. In addition, a number of investigators have been challenging the current thrice-weekly, diffusion-based treatment paradigm and have been developing approaches to emulate the function of natural kidneys. Thus an ideal care delivery model would focus on the holistic needs of the patient with kidney disease, while the ideal form of renal replacement therapy would mimic native kidneys, operating continuously, removing solutes with a molecular-weight spectrum similar to that of native kidneys, removing water and solutes on the basis of individual patient needs, and would be biocompatible, wearable, and ideally implantable. It would also be low cost, reliable, and safe. A few years ago, these technical requirements would have seemed impossible to achieve, but with advances in the sciences of nanotechnology and microfluidics, renal replacement of the future may come closer to this ideal.

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30

Rabin, Pauline L., and William J. Stone. End-Stage Renal Disease: An Integrated Approach. Elsevier Science & Technology Books, 2013.

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31

Haddad, Maha N., Erica Winnicki, and Stephanie Nguyen. Adolescents with Chronic Kidney Disease: From Diagnosis to End-Stage Disease. Springer, 2018.

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32

Haddad, Maha N., Erica Winnicki, and Stephanie Nguyen. Adolescents with Chronic Kidney Disease: From Diagnosis to End-Stage Disease. Springer, 2019.

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33

Sarwal, Minnie M., and Ron Shapiro. Paediatric renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0290.

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Approximately 1 in 65,000 children develops end-stage renal disease (ESRD) each year with almost 1200 children (aged 0–19 years) in the United States developing ESRD annually. Kidney transplantation is the primary method of treating ESRD in the paediatric population. The special issues in children and adolescents with ESRD include achieving normal growth and cognitive development. This chapter discusses the advances in surgical techniques, patient selection, transplant evaluation/preparing for transplantation, postoperative management (including fluid management in infants and small children), and the evolution of immunosuppressive drugs that have resulted in improved quality of life and a reduction in the mortality rate of children with chronic renal failure.

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34

1933-, Friedman Eli A., and Mallappallil Mary C, eds. Present and future therapies for end-stage renal disease. New Jersey: World Scientific, 2010.

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35

Joseph, Loscalzo, and London Gérard M, eds. Cardiovascular disease in end-stage renal failure. Oxford: Oxford University Press, 2000.

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36

Winston, Jonathan, Etti Zeldis, John A. Grimaldi, and Esteban Martínez. HIV-Associated Nephropathy, End-Stage Renal Disease, Dialysis, and Kidney Transplant. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0044.

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Antiretroviral therapy has changed the phenotype of HIV-related kidney disease to a more chronic disease model. In addition to HIV-associated nephropathy (HIVAN), patients with HIV may experience kidney dysfunction related to other chronic illnesses, such as diabetes, hypertension, and hepatitis C. Patients with HIV should be monitored for the development of chronic kidney disease and the potential nephrotoxicity of antiretroviral therapy. For patients with HIV who progress to end-stage renal disease, the outcomes on dialysis and management of the dialysis procedure are similar to the outcomes of patients without HIV. Renal transplantation is a promising treatment option for HIV patients with end-stage renal disease, despite certain barriers inherent in the transplant evaluation process. Concomitant HIV and end-stage renal disease, with the stress of dialysis, can exacerbate psychiatric illness.

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37

Ponticelli, Claudio, and Richard J. Glassock, eds. Treatment of Primary Glomerulonephritis. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784081.001.0001.

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Primary glomerulonephritis is one of the most common kidney diseases, and a main cause of end-stage renal disease (ESRD). Glomerulonephritis has multiple subtypes, each with different physiopathologies, clinical presentation, and management requirements, which makes treatment difficult. As a complex set of diseases, the choice of symptomatic and specific treatment is critical to ameliorating the relentless course of glomerulonephritis. Focusing on all subtypes of primary glomerulonephritis, from epidemiology and classification, to pathogenesis and treatment, this volume includes the latest research and evidence-based practice. With a strong emphasis on drugs used for both symptomatic and specific treatments, the mechanisms of action, effectiveness, and potential toxicity are considered for therapeutic strategies in the different subtypes of primary glomerulonephritis. Each chapter follows a clear and logical format that allows easy access to key information, and provides extensive references for further information.

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38

A clinical guide to nutrition care in end-stage renal disease. 2nd ed. Chicago, Ill: American Dietetic Association, 1994.

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39

A Clinical guide to nutrition care in end-stage renal disease. Chicago, Ill: American Dietetic Association, 1987.

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40

Wenzel, Ulrich, Thorsten Wiech, and Udo Helmchen. The effect of hypertension on renal vasculature and structure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0211.

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The concept of hypertensive nephrosclerosis was introduced by Volhard and Fahr in 1914 and has been extensively used in the literature since then, but its existence is controversial. While it is indisputable that malignant hypertension is a cause of end-stage renal disease (ESRD), there remains controversy as to whether the so-called benign nephrosclerosis can also lead to ESRD.Pressure, if it is great enough, will eventually disrupt any structure. Obviously, this is also true of blood pressure. It is therefore not surprising that an experimentally induced great increase in pressure disrupts the integrity of the blood-vessel wall. Such vascular lesions may be caused or at least influenced by several factors: humoral factors such as angiotensin II, catecholamines, mineralocorticoids, and vasopressin may increase vascular permeability, thereby damaging the vessel walls independently of, or superimposed upon, elevated blood pressure.Nephrosclerosis (literally, hardening of the kidney, Greek derivation: nephros, kidney; sclerosis, hardening) refers to diseases with predominant pathological changes occurring in the pre-glomerular vasculature and secondary changes involving the glomeruli and interstitium. Therefore, it is appropriate to describe first those vascular lesions, which, at least under defined experimental conditions, are believed to be caused solely by the presence of hypertension.

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41

Theofilou, Paraskevi, ed. Outcomes Assessment in End - Stage Kidney Disease - Measurements and Applications in Clinical Practice. BENTHAM SCIENCE PUBLISHERS, 2013. http://dx.doi.org/10.2174/97816080573511130101.

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42

Sevelamer in patients with end-stage renal disease: A systematic review and economic evaluation. Ottawa: Canadian Agency for Drugs and Technologies in Health, 2006.

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43

Halper, Thomas. Misfortunes of Others: End-Stage Renal Disease in the United Kingdom. Cambridge University Press, 2009.

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44

1938-, Hardy Mark A., and Kutscher Lillian G, eds. Positive approaches to living with end stage renal disease: Psychosocial and thanatologic aspects. New York: Praeger, 1986.

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45

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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46

Kramer, W., and V. Wizemann. The Heart in End-Stage Renal Failure: Etiology, Symptoms and Management of Uremic Heart Disease (Contributions to Nephrology). S Karger Pub, 1987.

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47

Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.

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48

(Editor), Mark A. Hardy, Gerald B. Appel (Editor), John M. Kiernan (Editor), Austin H. Kutscher (Editor), Martha L. Orr (Editor), Carol Smith Torres (Editor), and Lissa Parsonnet (Editor), eds. Positive Approaches to Living with End Stage Renal Disease: Psychosocial and Thanatalogic Aspects (The Foundation of Thanatology Series). Praeger Publishers, 1986.

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49

Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.

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50

Yaqoob, Muhammad M. Acidosis in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0148.

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Metabolic acidosis becomes increasingly common as chronic kidney disease progresses. It is associated with a number of complications, including bone disease, altered protein synthesis and degradation, skeletal muscle wasting, and lately progressive glomerular filtration rate loss. Experimental and clinical studies suggest a role for alkali therapy to lessen these complications. Recent controlled studies support this notion, and suggest that correction of metabolic acidosis in patients with chronic kidney disease slows the rate of decline of renal function and the development of end-stage renal disease, although more definitive evidence is needed on the long-term benefits of alkali therapy, type of alkali supplements, and the optimal level of serum bicarbonate.

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