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1
S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.
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2
S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.
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3
S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.
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4
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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5
S, Parfrey Patrick, and Harnett John D, eds. Cardiac dysfunction in chronic uremia. Boston: Kluwer Academic Publishers, 1992.
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6
Keenan, Emma W. Kidney patients' wellness diet--tasty recipes: Low protein, low potassium, low sodium, and low fat diet : combined renal and triglyceride diet. Virginia Beach, Va: Grunwald and Radcliff, 1986.
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7
Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Incorporated, John, 2008.
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8
Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Incorporated, John, 2008.
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9
Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Limited, John, 2007.
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10
Bakris, George L. Kidney in Heart Failure. Springer London, Limited, 2012.
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11
(Contributor), Khalid Ashai, William Cohn (Contributor), Matthew Forrester (Contributor), Kelly Guglielmi (Contributor), Charles Herzog (Contributor), Rosemary Kelly (Contributor), Rakhi Khanna (Contributor), et al., eds. Cardiac Surgery in Chronic Renal Failure: Clinical Management and Outcomes. Blackwell Publishing Limited, 2007.
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12
The Kidney in Heart Failure. Springer, 2012.
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13
Bakris, George L. The Kidney in Heart Failure. Springer, 2012.
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14
Bakris, George L. The Kidney in Heart Failure. Springer, 2014.
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15
Cardiac Dysfunction in Chronic Uremia (Topics in Renal Medicine). Springer, 1991.
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16
Bakris, George L. Managing the Kidney When the Heart Is Failing. Springer London, Limited, 2012.
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17
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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18
Parfrey, Patrick S. Cardiac Dysfunction in Chronic Uremia. Springer, 2012.
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19
Bakris, George L. Managing the Kidney when the Heart is Failing. Springer, 2012.
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20
Managing The Kidney When The Heart Is Failing. Springer, 2012.
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21
Cruz, Dinna N., Anna Giuliani, and Claudio Ronco. Acute kidney injury in heart failure. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0248.
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Acute kidney injury (AKI) occurring during heart failure (HF) has been labelled cardiorenal syndrome (CRS) type 1. CRS is defined as a group of ‘disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other’. This consensus definition was proposed by the Acute Dialysis Quality Initiative, with the aim to standardize those disorders where cardiac and renal diseases coexist. Five subtypes have been proposed, according to which organ is affected first (cardiac vs renal) and whether the dysfunction is acute or chronic. Another subtype which includes systemic conditions leading to both heart and kidney dysfunction is also described.The term ‘worsening renal function’ has been regularly used to describe the acute and/or subacute changes that occur in the kidneys following HF. However, the AKI classification according to the current consensus definition better represents the entire spectrum of AKI in the setting of HF.The pathophysiology of heart–kidney interaction is complex and still poorly understood. Factors beyond the classic haemodynamic mechanisms appear to be involved: neurohormonal activation, venous congestion, and inflammation have all been implicated.Diuretics are still a cornerstone in the management of HF. Intravenous administration by bolus or continuous infusion appears to be equally efficacious. Biomarkers and bioelectrical impedance analysis can be helpful in estimating the real volume overload and may be useful to predict and avoid AKI. The role of ultrafiltration remains controversial, and it is currently recommended only for diuretic-resistant patients as it has not been associated with better outcomes. The occurrence of AKI during HF is associated with substantially greater short- and long-term mortality.
22
Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.
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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘cardiorenal syndrome’, in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration, still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin is a recently developed and very promising new biomarker for the diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.
23
Farmakis, Dimitrios, John Parissis, George Papingiotis, and Gerasimos Filippatos. Acute heart failure. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0051_update_001.
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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4–7%, a 2–3-month post-discharge mortality of 7–11%, and a 2–3-month readmission rate of 25–30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia.
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Farmakis, Dimitrios, John Parissis, and Gerasimos Filippatos. Acute heart failure: epidemiology, classification, and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0051.
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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2-3-month post-discharge mortality of 7-11%, and a 2-3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have a preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia. Different classification systems have been proposed for acute heart failure, reflecting the clinical heterogeneity of the syndrome; the categorization to acutely decompensated chronic heart failure vs de novo acute heart failure and to hypertensive, normotensive, and hypotensive acute heart failure are among the most widely used and clinically relevant classifications. The pathophysiology of acute heart failure involves several pathogenetic mechanisms, including volume overload, pressure overload, myocardial loss, and restrictive filling, while several cardiovascular and non-cardiovascular causes or precipitating factors lead to acute heart failure through a single of these mechanisms or a combination of them. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is the hallmark of acute heart failure, resulting from fluid retention and/or fluid redistribution. Myocardial injury and renal dysfunction are also involved in the precipitation and progression of the syndrome.
25
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.
26
Bell, Melissa. Heart and Soul: The Emotional Autobiography of Melissa Bell, Alexandra Burke's Mother. Blake Publishing, Limited, John, 2010.
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27
Heart and Soul: The Emotional Autobiography of Melissa Bell, Alexandra Burke's Mother. Blake Publishing, Limited, John, 2010.
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28
Zoccali, Carmine, Davide Bolignano, and Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.
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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
29
Cardiovascular Aspects of Dialysis Treatment: The Importance of Volume Control. Springer, 2000.
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30
Jardine, Alan G., and Rajan K. Patel. Lipid disorders of patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0102.
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The risk of developing cardiovascular (CV) disease is increased in patients with chronic kidney disease (CKD) and although dyslipidaemia is a major contributory factor to the development of premature CV disease, the relationship is complex. Changes in lipid fractions are related to glomerular filtration rate and the presence and severity of proteinuria, diabetes, and other confounding factors. The spectrum of CV disease changes from lipid-dependent, atheromatous coronary disease in early CKD to lipid-independent, non-coronary disease, manifesting as heart failure, and sudden cardiac death in advanced and end-stage renal disease. Statin-based lipid-lowering therapy is proven to reduce coronary events across the spectrum of CKD. The relative reduction in overall CV events, however, diminishes as CKD progresses and the proportion of lipid-dependent coronary events declines. There is nevertheless a strong argument for the use of statin-based therapy across the spectrum of CKD. The argument is particularly strong for those patients with progressive renal disease who will eventually require transplantation, in whom preventive therapy should start as early as possible. The SHARP study established the benefits and endorses the use of lipid-lowering therapy in CKD 3-4 but uncertainty about the value of initiation of statin therapy in CKD 5 remains. There is, however, no rationale for stopping agents started earlier in the course of the illness for compelling indications, particularly in those who will ultimately be transplanted. The place of high-density lipoprotein-cholesterol raising and triglyceride lowering therapy needs to be assessed in trials. Modifying dyslipidaemia in CKD has demonstrated that lipid-dependent atheromatous cardiovascular disease is only one component of the burden of CV disease in CKD patients, that this is proportionately less in advanced CKD, and that modification of lipid profiles is only one part of CV risk management.
31
Ostermann, Marlies, and Ruth Y. Y. Wan. Diuretics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0058.
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Fluid overload and chronic hypertension are the most common indications for diuretics. The diuretic response varies between different types and depends on underlying renal function. In patients with congestive heart failure, diuretics appear to reduce the risk of death and worsening heart failure compared with placebo, but their use in acute decompensated heart failure is questionable. Diuretics are also widely used in chronic kidney disease to prevent or control fluid overload, and treat hypertension. In acute kidney injury, there is no evidence that they improve renal function, speed up recovery, or change mortality. In patients with chronic liver disease and large volume ascites, paracentesis is more effective and associated with fewer adverse events than diuretic therapy, but maintenance treatment with diuretics is indicated to prevent recurrence of ascites. Mannitol has a role in liver patients with cerebral oedema and normal renal function. The use of diuretics in rhabdomyolysis is controversial and restricted to patients who are not fluid deplete. In conditions associated with resistant oedema (chronic kidney disease, congestive heart failure, chronic liver disease), combinations of diuretics with different modes of action may be necessary. Diuresis is easier to achieve with a continuous furosemide infusion compared with intermittent boluses, but there is no evidence of better outcomes. The role of combination therapy with albumin in patients with fluid overload and severe hypoalbuminaemia is uncertain with conflicting data.
32
Gardiner, Matthew D., and Neil R. Borley. Core surgical skills and knowledge. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199204755.003.0015.
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This chapter begins by discussing the basic principles of fluid and electrolyte homeostasis, fluid therapy, healthcare-associated infection, microorganisms and antimicrobials, preoperative assessment, and acute pain, before focusing on the key areas of knowledge, namely deep venous thrombosis, pulmonary embolism, respiratory tract infection, asthma, chronic obstructive pulmonary disease, acute respiratory failure, ischaemic heart disease, heart failure, cardiac arrhythmias, hypertension, diabetes mellitus, acute renal failure, stroke, acute confusional state, and haematological conditions. The chapter concludes with relevant case-based discussions.
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Vester, Udo, and Stefanie Weber. Townes–Brocks syndrome. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0359.
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Townes–Brocks syndrome (TBS) is an autosomal dominant disease with variable expression. Classical features are imperforate anus, dysplastic ears with congenital hearing deficit, and triphalangeal thumbs in most cases. A variety of other malformations (renal, genitourinary, heart, central nervous system, eyes) or hypothyroidism has been described. Mutations in SALL1 have been identified in patients with TBS and genetic testing allows confirmation of the diagnosis. Familiar and sporadic forms (caused by de novo mutations) seem to be equally distributed. Renal involvement in TBS is not uncommon and includes renal agenesis, hypo-/dysplasia, and renal cysts and may eventually lead to chronic renal failure. As renal function may not deteriorate before adulthood, renal function should be monitored in all patients. As cases with TBS can be oligosymptomatic, TBS should be suspected in every case with unexplained renal failure, minor abnormalities, or indicative family history. Genetic counselling is mandatory in identified cases.
34
Kierans, Ciara. Chronic Failures: Kidneys, Regimes of Care, and the Mexican State. Rutgers University Press, 2019.
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35
Kierans, Ciara. Chronic Failures: Kidneys, Regimes of Care, and the Mexican State. Rutgers University Press, 2019.
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36
Kierans, Ciara. Chronic Failures: Kidneys, Regimes of Care, and the Mexican State. Rutgers University Press, 2019.
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37
Fagard, Robert, Giuseppe Mancia, and Renata Cifkova. Blood pressure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0014.
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Prevention of hypertension can help prevent cardiovascular disease and renal complications. Obesity, a high sodium and low potassium intake, physical inactivity, and high alcohol consumption all contribute to the development of hypertension, and randomized controlled trials have shown that appropriate lifestyle modifications are able to reduce blood pressure and/or prevent the development of hypertension. The major complications of hypertension are stroke, coronary heart disease, heart failure, peripheral artery disease, and chronic kidney disease. Multiple randomized controlled trials and their meta-analyses have shown that treatment with antihypertensive drugs reduces the incidence of fatal and non-fatal cardiovascular events. In addition, meta-analyses have shown that there are no clinically relevant differences in the effects of the five major drug classes on outcome, so all of them are considered suitable for the initiation and maintenance of antihypertensive therapy. Nevertheless, the therapeutic approach in the elderly, women, and patients with diabetes, cerebrovascular, cardiac, or renal disease deserves special attention.
38
Wald, Ron, and Ziv Harel. The Long-Term Outcomes of Acute Kidney Injury. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0015.
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Recent research has provided important insights on the long-term outcomes of patients who develop acute kidney injury (AKI) in the setting of critical illness. Large epidemiologic studies have demonstrated compelling associations between episodes of AKI and progressive kidney disease and death, respectively, although such studies do not establish causality due to the potential for confounding. Whether AKI is intrinsically toxic or a mere by-product of serious comorbidities (e.g. prior chronic kidney disease, heart failure, diabetes), there is no doubt that AKI survivors are a high-risk group who would likely benefit from close post-discharge follow-up. Recent studies have shown that a minority of patients with AKI receive specialized nephrology follow-up after discharge, suggesting an opportunity for quality improvement. Emerging research is evaluating factors that predict chronic kidney disease, end-stage renal disease, and death among AKI survivors. This work will, it is hoped, suggest new targets for prevention and treatment, with the goal of enhancing the likelihood of recovery following AKI.
39
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0076.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
40
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_001.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
41
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_002.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
42
Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.
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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). Urinalysis may be normal or show low-grade proteinuria (< 1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
43
Lapsia, Vijay, Bernard Jaar, and A. Ahsan Ejaz, eds. Kidney Protection. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190611620.001.0001.
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Kidney disease is a crippling disease that affects approximately ten percent of the population worldwide, with more than 2.6 million individuals estimated to receive renal replace therapy. Chronic kidney disease (CKD) is fast becoming a major public health issue even in resource poor settings, with some estimates predicting a disproportionate increase in countries such as China and India. Consequently, renal protection has become a vital and critical component of prevention. While observational data suggests that awareness remains low, the concept of renal protection is currently under-recognized in promoting recovery as well as preventing further renal loss. Kidney Protection: Strategies for Renal Preservation is a clinically applicable review of the current medical care and research that aims to address the awareness gap. The authors combine renal protection research and clinical practices with an interdisciplinary approach that is inclusive of nephrology,urology, critical care, anesthesia, emergency medicine and clinical medicine.Written by experts in the field of nephrology, the authors have also included applicable photographs and line drawings. The specific topics covered include: protection of the kidneys in hypertension, diabetes and heart disease, exposure to contrast including coronary angiogram, atherosclerosis, and more. This handbook is formatted to emphasize clinical practice points and major systemic illnesses. Additionally, it features the latest evidence-based practice guidelines for optimal renal outcomes, thus, making it a concise reference for the busy clinician interested in understanding the basics of kidney disease assessment, renal injury prevention, and renal preservation.
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Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.
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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
45
Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0336.
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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide, which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, gut, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic. The disease is commonly diagnosed in children and young men often after some years of usually neuropathic symptoms, with exacerbations (Fabry crises), that commonly elude diagnosis for a long time. These usually occur years in advance of overt involvement of other organs. Diagnosis may also be suspected from renal biopsy, echocardiographic evidence of cardiomyopathy commonly beginning as left ventricular hypertrophy, or characteristic angiokeratomas typically in ‘bathing trunk’ distribution on skin. Renal manifestations are of proteinuria leading to progressive chronic kidney disease associated with deposits in podocytes. Diarrhoea is common. Disordered sweating is typical. Corneal lesions are also typical and there may be tortuosity of retinal vessels. Strokes are increased in frequency, and sensorineural deafness may occur. Women have fewer and later overt manifestations but some develop severe disease.
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Grant, Robert. Neurocutaneous syndromes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0235.
Full textAbstract:
This chapter describes several neurocutaneous syndromes, including tuberous sclerosis, neurofibromatosis, Sturge–Weber syndrome, Von-Hippel–Lindau disease and ataxia telangiectasia amongst others.Tuberous sclerosis, also known as Epiloia or Bournville’s Disease, is an autosomal dominant multisystem disease it usually presents in childhood with a characteristic facial rash, adenoma sebaceum, seizures, and sometimes learning difficulties. Central nervous system lesions in tuberous sclerosis are due to a developmental disorder of neurogenesis and neuronal migration. Other organs such as the heart and kidney are less commonly involved. The condition has very variable clinical expression and two-thirds of cases are thought to be new mutations, therefore it is important to examine and screen relatives. Management may involve many specialists and close co-operation between specialists is essential.The neurofibromatoses are autosomal-dominant neurocutaneous disorders that can be divided into ‘peripheral’ and ‘central’ types, although there is significant overlap. The characteristic features of neurofibromatosis type 1 are café au lait spots, neurofibromas, Lisch nodules, osseous lesions, macrocephaly, short stature and mental retardation, axillary freckling, and associations with several different types of tumours.Sturge–Weber syndrome involves a characteristic ‘port-wine’ facial naevus or angioma associated with an underlying leptomeningeal angioma or other vascular anomaly. It affects approximately 1/20 000 people. There can be seizures, low IQ, and underlying cerebral hemisphere atrophy as a result of chronic state of reduced perfusion and increased oxygen extraction. Patients may present with focal seizures which are generally resistant to anticonvulsant medication and can develop glaucoma.Von-Hippel– Lindau disease is one of the most common autosomal-dominant inherited genetic diseases that are associated with familial cancers. Von-Hippel–Lindau disease is characterized by certain types of central nervous system tumours, cerebellar and spinal haemangioblastomas, and retinal angiomas, in conjunction with bilateral renal cysts carcinomas or phaechromocytoma, or pancreatic cysts/islet cell tumours (Neumann and Wiestler 1991).Other neurocutaneous syndromes discussed include Hypomelanosis of Ito, Gorlin syndrome, Sjogren–Larsson syndrome, Proteus syndrome, Hemiatrophy and hemihypertrophy, Menke’s syndrome, Xeroderma pigmentosum and Cockayne’s syndrome.