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1
Sprague, Stuart M., and Menaka Sarav. Chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0115_update_001.
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The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyroidism. Renal osteodystrophy involves pathologic changes of bone morphology related to progressive CKD and is quantifiable by histomorphometry, based on bone biopsy. CKD-MBD is associated with significant morbidity, including bone loss, fractures, cardiovascular disease, immune suppression, as well as increased mortality. As the disorder begins early in the course of CKD, a proactive approach with intervention is important. Therapeutic strategies could then be employed to prevent and correct these disturbances, aiming to improve cardiovascular outcomes and survival. Current practice guidelines for CKD-MBD are based on insufficient data and high-quality studies are required before specific treatment can be advocated strongly.
2
Christensen, Alan J., Julia R. Van Liew, and Quinn D. Kellerman. Depression in Chronic Kidney Disease. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.013.
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Chronic kidney disease (CKD) is a prevalent medical condition posing a range of unique physical and self-management demands for patients and presenting a variety of patient management challenges for clinicians. Co-morbid depression and other psychiatric disorders represent a significant detriment to the quality of life and clinical outcomes of CKD patients. Evidence suggests that 12% to 40% of individuals in the later stages of CKD meet DSM (III, IV, or IV-TR) diagnostic criteria for a mood disorder. Moreover, the existence of comorbid depression has been associated with earlier patient mortality. Depression assessment is itself complicated by the physiologic and medical treatment status of the patient, and depression is believed to be both underdiagnosed and undertreated in this population. Rigorous empirical demonstrations of the safety and/or efficacy of both pharmacologic and nonpharmacologic treatments for depression are limited for this population. However, a number of important factors that should be considered in treating depression in kidney disease patients have been identified. This chapter summarizes these and other key clinical recommendations relevant to the evaluation and treatment of co-morbidity of depression in this population.
3
Hutchison, Alastair J., and Michael L. Picton. Fractures in patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0121.
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Patients with any degree of chronic kidney disease (CKD) have a much higher risk of fractures than the general population, and the risk of death at 1 year post hip fracture in a dialysis patient is over 60%, compared to less than 20% for a non-CKD patient. The assessment of fracture risk and diagnosis of the underlying skeletal pathology in CKD patients is a significant clinical challenge. Non-invasive imaging techniques are not totally reliable in the general population, and the presence of advanced CKD (stages 4, 5, and 5D) renders them largely useless. Bone strength is not determined only by quantity of bone, and renal osteodystrophy can significantly affect bone quality, rendering it liable to fracture even in the presence of a normal bone density measurement. Currently, the only reliable method of assessing both quantity and quality of bone is the examination of trans-iliac bone biopsy, which is generally, but probably incorrectly, perceived to be overly invasive. However, identifying the cause of reduced bone strength and fractures may influence the choice of therapy. For example, in the presence of low-turnover states such as adynamic bone, antiresorptive agents may be ineffective. Pharmaceuticals licensed for the treatment of osteoporosis in the general population can be used similarly in patients with CKD 1–3 without dosage alteration. In CKD 4, post-hoc analyses suggest denosumab is effective and safe, based on a 3-year study that included 73 such patients. In CKD 5 and 5D no dependable data exists to guide therapy, and it should probably be reserved for patients who have already suffered and survived a fracture, and are therefore at high risk of death from a second event.
4
Malyszko, Jolanta, and Iain C. Macdougall. Iron metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0125.
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While whole-body (‘absolute’) iron deficiency is common and probably increased in frequency in chronic kidney disease (CKD), functional iron deficiency is a particular problem in CKD. Absolute iron deficiency is likely to be present in advanced CKD when the ferritin falls below 100 ng/mL and the TSAT falls below 20%. Functional iron deficiency is characterized by the presence of adequate iron stores (as defined by conventional criteria), but with an inability to mobilize this iron rapidly enough to adequately support erythropoiesis with the administration of erythropoietin. Among such patients, the serum ferritin level is either normal or elevated (usually between 100 and 800 ng/mL), with a TSAT typically ≤20%. Hepcidin, a novel peptide discovered at the turn of the twenty-first century, is an iron gatekeeper that plays a key role in functional iron deficiency, and the ‘anaemia of chronic disease’. The main function of hepcidin is homeostatic regulation of iron metabolism and mediation of host defence and inflammation. Hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from the macrophages. Novel strategies that modulate hepcidin and its target ferroportin for the treatment of anaemia of chronic diseases are currently undergoing extensive research.
5
Biggar, Patrick, Hansjörg Rothe, and Markus Ketteler. Epidemiology of calcium, phosphate, and parathyroid hormone disturbances in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0109_update_001.
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Chronic kidney disease-mineral and bone disorders (CKD-MBD), calcium, phosphate, and parathyroid hormone are biomarkers of mortality and cardiovascular risk. Hyperphosphataemia is a prominent and pathophysiologically most plausible risk indicator. Calcium balance and load appear to be more important than serum concentrations. Parathyroid hormone is a less reliable marker with a relatively wide range extending above that applicable for a normal population especially when used as a singular laboratory parameter without additional assessment of bone metabolism, for example, bone-specific alkaline phosphatase and bone biopsy. There is not a single prospective controlled hard-outcome study that provides us with unequivocal evidence that such an isolated laboratory parameter-based treatment approach will lead to significant clinical improvements. As CKD-MBD is complex, clinical decisions would be made easier by informative prospective trials.
6
Voinescu, Alexandra, Nadia Wasi Iqbal, and Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.
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In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.
7
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.
8
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.
9
Comorbidities in Chronic Kidney Disease (CKD). MDPI, 2021. http://dx.doi.org/10.3390/books978-3-03936-669-9.
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10
Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Chronic kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0163.
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Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, where the abnormalities have been present for >3 months and have implications for health. It is characterized by a reduced estimated glomerular filtration rate (eGFR) or other renal abnormalities. CKD is staged according to the eGFR or the degree of albuminuria. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for CKD is either an eGFR that is <60 ml/min 1.73 m−2 and has been present for >3 months, or one or more markers of kidney damage, when these have been present for >3 months.
11
Upadhyay, Ashish, Lesley A. Inker, and Andrew S. Levey. Chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0094.
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The conceptual model, definition, and classification of chronic kidney disease (CKD) were first described in the National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines in 2002 and have had a major impact on patient care and research. Since this publication there has been an increased recognition that the cause of CKD influences progression and complications. In addition, epidemiologic reports from diverse populations have consistently shown graded relations between higher albuminuria and adverse kidney outcomes and complications, in addition to, and independent of, low GFR. Given these new understanding in risk relationships, Kidney Disease Improving Global Outcomes (KDIGO) updated the original guidelines in 2012. The updated guidelines retain the KDOQI definition of CKD, but recommend classifying CKD by the cause, level of GFR, and level of urinary albumin to creatinine ratio. Specialized nephrology care is recommended for severe reduction in GFR or high albuminuria, uncertain diagnosis, or difficult to manage complications.
12
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.
13
Goldsmith, David J. Cardiovascular disease and chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0098.
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Even after as full a statistical adjustment as can be made for traditional cardiovascular risk factors has been undertaken, impaired kidney function and raised concentrations of albumin in urine each increase the risk of cardiovascular disease (CVD) by two- to fourfold, the degree increasing with severity. If the patient is also suffering from diabetes (as either the cause of CKD or a complication of it), the risks of CVD increase two- to fourfold again. CKD patients should, therefore, be acknowledged as having perhaps the highest cardiovascular risk of any patient cohort. CVD is underdiagnosed and undertreated in these patients. In early CKD the manifestations of CVD are similar to those of other patients. In late CKD and particularly in patients on dialysis the epidemiology is different. Left ventricular hypertrophy is very common and sudden cardiac death is greatly increased in incidence. Heart failure is a common complication. Calcification of valves and vessels becomes increasingly common and bad CVD outcomes are associated with hyperphosphataemia and other manifestations. The mechanisms by which risks are increased are not fully understood. The evidence base for the effectiveness of established therapies for CVD is relatively light in patients with CKD, but there is evidence for benefit of lipid-lowering therapies and most nephrologists believe that blood pressure and volume control are important for good long-term outcomes. Evidence of impact on CVD of interventions to alter mineral bone disease is disappointingly weak.
14
Beaulieu, Monica, Catherine Weber, Nadia Zalunardo, and Adeera Levin. Chronic kidney disease long-term outcomes. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0097.
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Chronic kidney disease (CKD) is associated with a variety of outcomes, some of which are directly and indirectly related to kidney disease, but which ultimately impact on patients’ quality of life and long-term outcomes. The events to which people with CKD are exposed ultimately determine their risk and prognosis of both progression to needing renal replacement therapy, or other morbidities and mortalities. The notion of competing risk is important. The five major outcomes of CKD are: progression of CKD, progression to ESRD (either dialysis or transplantation); death; cardiovascular events; infections; and hospitalizations. Where data is available, not only the risk of the specific outcome, but the factors which may predict those outcomes are described. Each section describes what is currently known about the frequency of the outcome, the limitations of that knowledge, the risk factors associated with outcome, and implications for care and future research. Available published literature often describes outcomes in CKD populations as if it is a homogenous group of patients. But it is well documented that outcomes in those with CKD differ depending on stage or severity, and whether they are or are not known to specialists. Where possible, each section ensures that the specific CKD cohort(s) from which the information is derived is clearly described.
15
Orth, Stephan R. Smoking in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0103.
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Smoking has been acknowledged as the number one preventable cause of death in most countries. The adverse effects of smoking on the kidney are less known. Prospective, population-based, observational studies, and evidence from experimental work indicate that smoking (a) is a relevant risk factor for chronic kidney disease (CKD) in the general population and (b) is associated with an increased risk of deterioration in renal function in CKD patients. The latter is especially true for patients with diabetic nephropathy or hypertensive renal damage. The conclusion is that smoking is an important renal risk factor and nephrologists should make greater efforts to motivate patients to stop smoking, not least because smoking cessation improves the prognosis of CKD.
16
Shrivastava, Seema, Beverley J. Hunt, and Anthony Dorling. Coagulopathies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0135.
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Coagulation abnormalities are common in chronic kidney disease (CKD). Both haemorrhage and thrombosis are more common than in the general population. Haemorrhage, when it occurs, is associated with increased morbidity and mortality compared to that seen in non-uraemic patients. It is more likely spontaneously, but particularly in association with anti-platelet agents or anticoagulants. The increased risk of both arterial and venous thrombosis occurs in part because of the increase prevalence of traditional risk factors for thrombosis in CKD, in part because of the specific problems associated with nephrotic syndrome, and also because of specific putative prothrombotic factors associated with CKD, such as increased levels of coagulation factors and altered platelet function associated with uraemia. Two syndromes, both characterized by intravascular thrombosis can contribute to the development of CKD. The first is antiphospholipid syndrome, due to the presence of antibodies against negatively charged phospholipids, in which thrombosis of the renal vasculature is relatively common. The second is a group of conditions, the thrombotic microangiopathies, in which inherited or acquired deficiencies of ADAMTS13, antiphospholipid antibodies, or pathological endothelial cell activation in renal vessels, sometimes due to functional deficiencies of one or more proteins regulating coagulation or complement activation, leads to acute renal dysfunction associated with anaemia.
17
Zhang, Luxia, and Haiyan Wang. Chronic kidney disease in developing countries. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0096_update_001.
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The spread of non-communicable diseases (NCDs) is a barrier to the development of goals including reduction of poverty, health equity, economic stability, and human security. NCDs accounted for 61% of the estimated 58 million deaths and 46% of the global burden of diseases worldwide in 2005. Among NCDs, chronic kidney disease (CKD) is of particular significance. It is recognized that the burden of CKD is not only limited to its impact on demands for renal replacement therapy but has equally major impacts on the health of the overall population. For example, it is now well established that among the general population as well as in the diabetic or hypertensive population, the prognosis, especially the mortality and acceleration of cardiovascular events, depends on kidney involvement. Also, CKD is associated with other major serious consequences including increased risk of acute kidney injury, increased risk of mineral and bone disease, adverse metabolic and nutritional consequences, infections, and reduced cognitive function. As a consequence of these amplifying effects, the financial expenditure and medical resources consumed for the management of CKD patients is much higher than expected. The burden of CKD is likely to have profound socioeconomic and public health consequences in developing countries.
18
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.
19
Carrero, Juan Jesús, Hong Xu, and Bengt Lindholm. Diet and the progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0101.
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The dietary management of non-dialysed CKD patients has focused on limiting the intake of substances which lead to accumulation of urea, potassium, phosphorus, and sodium. Recent advances in nutritional epidemiology have given us the opportunity to examine the relationships between diet and CKD. This chapter focuses on evidence relating to retarding progression of renal impairment in the early to mid stages of CKD. Limits may need to change if GFR falls. The hypothesis that a high dietary protein intake leads to progressive CKD through a mechanism of glomerular hyperfiltration has been taught for decades, and it appears effective in animals. However, the evidence that low-protein diets (LPDs) halt CKD progression in patients is weak. Their management is of course likely to include other interventions such as blood pressure control. There is risk to low-protein diets. There is some evidence that high protein intakes are harmful. We therefore recommend moderate protein intake (not low; not high – no protein supplements; around 1g/kg/day). Salt handling is impaired in most patients with CKD, probably even early stages, and hypertension is an early feature, except in salt-losing patients, to whom different rules apply. Salt intake tends to raise blood pressure, worsen proteinuria, and reduce the effects of angiotensin converting enzyme inhibitors on blood pressure and proteinuria. Very low salt intakes are difficult to comply with and limit diet. In early stages of CKD we therefore recommend restriction to moderately low levels (below 6g/day of salt; 100 mmol of sodium). Lower levels may have additional benefits, and these limits may need to be reduced as GFR declines. Potassium is associated with healthy, desirable foods such as fruit and vegetables. It should only be restricted if high serum values make this necessary.
20
Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.
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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.
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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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Bramham, Kate, and Catherine Nelson-Piercy. Pregnancy in patients with chronic kidney disease and on dialysis. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0295_update_001.
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Chronic kidney disease (CKD) affects a small but increasing minority of women becoming pregnant. It is associated with additional risks depending on pre-pregnancy glomerular filtration rate, proteinuria, and hypertension. Some drugs are contraindicated in pregnancy. These are powerful reasons for counselling all women of childbearing age about pregnancy in CKD. With minor CKD the main issue is moderately increased risk of pregnancy-associated hypertension and pre-eclampsia. More advanced CKD is associated with reduced fertility, progressively increased risk of pre-term delivery and a significant chance of permanent loss of maternal renal function. Distinguishing pre-eclampsia from the natural effects of pregnancy on manifestations of CKD can be challenging. Blood pressure targets may be modified during pregnancy and angiotensin converting enzyme inhibitors and angiotensin receptor blockers are contraindicated. Dialysis may be initiated if pregnancy occurs at advanced levels of CKD. Pregnancy may also occur in patients on dialysis, usually in women with some residual native renal function. More intensive dialysis may improve outcomes.
23
Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Screening for kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0353.
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Renal disease is common and, with routine reporting of estimated glomerular filtration rates, impairment of renal function is increasingly being recognized. As renal impairment is usually asymptomatic until very advanced, chronic kidney disease (CKD) guidelines have been developed to improve the identification and screening of at-risk populations. Target groups include patients with vascular risk factors (e.g. diabetes mellitus and hypertension); patients with certain multisystem diseases which can cause renal impairment; patients with urological conditions; patients on nephrotoxic medication; and immediate relatives of patients with established renal disease. Kidney function should also be checked during intercurrent illness and perioperatively in all patients with CKD or suspected CKD. The frequency of screening is dictated by the CKD stage.
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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.
25
Nikolov, Igor G. The New Kidney and Bone Disease: Chronic Kidney Disease - Mineral and Bone Disorder (CKD-MBD). INTECH Open Access Publisher, 2012.
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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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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.
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Andreucci, Michele, Jose Luis Gorriz, Carlo Garofalo, and Michele Provenzano, eds. Management of Patients With Non-Dialysis Dependent Chronic Kidney Disease (ND-CKD). Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-577-7.
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Gökmen, M. Refik, and Graham M. Lord. Aristolochic acid nephropathy caused by ingestion of herbal medicinal products. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0089.
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Aristolochic acid nephropathy (AAN) is a rapidly progressive renal disease caused by the ingestion of plant products containing aristolochic acid (AA), first described in connection with the use of Chinese herbal medicines. Although the true worldwide extent of this disease is unknown, it is likely to represent a significant cause of chronic kidney disease (CKD) in many parts of the world. Furthermore, recent data have also demonstrated that AA is also the primary aetiological agent in Balkan endemic nephropathy. AAN is notable in its association with urothelial malignancy, with the mechanisms of carcinogenesis now well characterized. Aside from a possible role for corticosteroid therapy in slowing disease progression in selected patients, no disease-specific treatments have yet been shown to alter the course of this nephropathy. Therefore, prevention of exposure to AA and, in affected patients, effective management of the risk of malignancy are key principles in the approach to this condition. Although preparations containing Aristolochia spp. and herbs that can be confused or substituted for Aristolochia have been banned in many countries, other herbal products containing AA have continued to be available to consumers long after these bans have been instituted, highlighting the ongoing need for awareness of this disease.
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Ferro, Charles J., and Khai Ping Ng. Recommendations for management of high renal risk chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0099.
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Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.
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Weaver, Virginia M., Bernard G. Jaar, and Jeffrey J. Fadrowski. Kidney Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0031.
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This chapter describes kidney disorders related to occupational and environmental exposures and addresses prevention and control. Sections address assessment of kidney function, acute kidney injury, and chronic kidney disease (CKD). Kidney disease from acute, high-level exposures as well as lower level exposures in combination with other CKD risk factors are considered. Established nephrotoxicants, including aristolochic acid, arsenic, cadmium, lead, melamine, mercury, silica, and solvents, are discussed. The limited data available on other agents, such as perfluorooctanoic acid and fine particulate matter, are also presented. The potential for kidney function to impact biomarker levels is considered. A final section addresses a current epidemic of CKD of unknown etiology in agricultural workers in specific countries.
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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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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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Vaziri, Nosratola D. Oxidative stress and its implications in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0112.
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Reactive oxygen species (ROS) are produced at low levels physiologically and their production conveys signals and has specific functions. Control mechanisms ensure that this does not cause damage. ROS are highly reactive and cytotoxic and are also deliberately produced by inflammatory cells (granulocytes, macrophages) to kill pathogens. If these chemicals are released inappropriately or excessively, or if control mechanisms are under-functioning, bystander or unintended tissue damage may be caused. The concept of oxidative stress is based on the idea that in certain states, commonly inflammatory states, release of oxygen radicals may be excessive, or control mechanisms weakened, so that tissue damage occurs. In CKD, both overproduction and diminished control may apply. No effective therapies acting via these pathways have been established so far though there remain some candidates.
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Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.
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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
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Freda, Benjamin J., and Gregory L. Braden. Other toxic acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0085.
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Chronic kidney disease (CKD) is often the result of incomplete recovery of renal function from a variety of causes of acute tubulointerstitial injury. Exposure to ethylene glycol, chlorinated hydrocarbons, paraquat, or toxic mushrooms often causes severe acute kidney injury (AKI), leading to chronic tubulointerstitial nephritis (TIN) and CKD, including end-stage renal disease. Ethylene glycol intoxication often leads to chronic TIN and CKD from direct renal tubular toxicity and from interstitial calcium oxalate deposition. Chlorinated hydrocarbon exposure can cause dialysis-dependent AKI, but only rarely causes CKD from interstitial calcium deposition. Paraquat intoxication causes dose-dependent AKI and often Fanconi syndrome in up to 50% of patients, but only 15% of these patients survive, so CKD is rarely seen as a complication. The toxic mushrooms Cortinarius and Amanita phalloides often cause delayed AKI leading to CKD, chronic dialysis, or renal transplantation.
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Elder, Grahame J. Metabolic bone disease after renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0288.
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Patients who undergo kidney transplantation have laboratory, bone, and soft tissue abnormalities that characterize chronic kidney disease mineral and bone disorder (CKD-MBD). After successful transplantation, abnormal values of parathyroid hormone, fibroblast growth factor 23, calcium, phosphate, vitamin D sterols, and sex hormones generally improve, but abnormalities often persist. Cardiovascular risk remains high and is influenced by prevalent vascular calcification, and fracture risk increases due to a combination of abnormal bone ‘quality’, compounded by immunosuppressive drugs and reductions in bone mineral density. Patients with well managed CKD-MBD before transplantation generally have a smoother post-transplant course, and it is useful to assess patients soon after transplantation for risk factors relevant to the general population and to patients with CKD. Targeted laboratory assessment, bone densitometry, and X-ray of the spine are useful for guiding therapy to minimize post-transplant effects of CKD-MBD. To reduce fracture risk, general measures include glucocorticoid dose minimization, attaining adequate 25(OH)D levels, and maintaining calcium and phosphate values in the normal range. Calcitriol or its analogues and antiresorptive agents such as bisphosphonates may protect bone from glucocorticoid effects and ongoing hyperparathyroidism, but the efficacy of these therapies to reduce fractures is unproven. Alternate therapies with fewer data include denosumab, strontium ranelate, teriparatide, oestrogen or testosterone hormone replacement therapy, tibolone, selective oestrogen receptor modulators, and cinacalcet. Parathyroidectomy may be necessary, but is generally avoided within the first post-transplant year. A schema is presented in this chapter that aims to minimize harm when allocating therapy.
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Kashani, Kianoush B., and Amy W. Williams. Renal Failure. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0473.
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Renal failure is caused by acute kidney injury or chronic kidney disease. Acute kidney injury (AKI) is a common, devastating complication that increases mortality and morbidity among patients with various medical and surgical illnesses. Also known as acute renal failure, AKI is a rapid deterioration of kidney function that results in the accumulation of nitrogenous metabolites and medications and in electrolyte and acid-base imbalances. This chapter discusses the definition, epidemiology, pathophysiology, and etiology of AKI; the clinical approach to patients with AKI; and the management of AKI. Chronic kidney disease (CKD) has been categorized into 5 stages. When renal function decreases to stage 3, the complications of CKD become evident. These complications include hypertension, cardiovascular disease, lipid abnormalities, anemia, metabolic bone disease, and electrolyte disturbances. To prevent the progression of CKD, therapy must be directed toward preventing these complications and achieving adequate glucose control in diabetic patients with CKD.
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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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Wiles, Kate, and Catherine Nelson-Piercy. Contraception in patients with kidney disease. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0293_update_001.
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Three per cent of women of childbearing age have chronic kidney disease, and although end-stage renal failure impacts on fertility, conception and high-risk pregnancy do occur. Following renal transplantation, the patient should understand the potential impact of a pregnancy on transplant function and vice versa. Surveys show that a large proportion of pregnancies in female renal patients are unplanned. The effectiveness of a particular contraceptive method is dependent upon acceptability to the patient and compliance. Contraceptive decision-making needs to balance acceptability and safety with the risk of an unplanned pregnancy. Oestrogen-containing contraceptive methods are considered unacceptable for many renal patients because of their association with increased blood pressure and thrombotic and vascular events. Progesterone-only methods have an advantageous safety profile. The progesterone-only pill (desogestrel preparations), intrauterine system (Mirena®), and implant (Nexplanon®) are safe and effective in women with CKD. Concerns regarding the intrauterine system (Mirena®) in women taking immunosuppression are unfounded and observational evidence does not demonstrate an increased risk of infection. Sterilization is effective and should be considered to be irreversible. The effectiveness of barrier methods is reduced when ‘typical use’ is compared to ‘perfect use’. Unplanned pregnancy rates are high with fertility awareness methods and reliance on lactational amenorrhoea is not advocated.Interactions between drugs which are commonly prescribed in the renal population and different contraceptive methods are outlined in this chapter.
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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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Davenport, Dr Andrew. Renal diseases and emergencies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00011.
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Chapter 11 discusses diseases and emergencies involving renal medicine, including investigation of the renal tract, acute kidney injury (AKI), haematuria and proteinuria, urinary tract infection (UTI), urinary tract obstruction, tumours of the renal tract, chronic kidney disease (CKD), and renal transplant patients.
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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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Rees, Lesley. Growth and development. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0291.
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Enabling achievement of full height potential in a child with chronic kidney disease (CKD) is one of the major and most challenging goals for the paediatric nephrologist. Short stature is associated with psychological maladjustment and with increased morbidity and mortality. The causes of poor growth are multifactorial and include poor nutrition, and metabolic, haematological, and endocrine disturbances. The most vulnerable times are the periods of most rapid growth, that is, infancy and puberty. Growth during infancy is principally dependent on nutrition so many infants need supplemental enteral feeding. Growth delay correlates with severity of CKD, with those on dialysis faring the worst such that by CKD stage 5, approximately 25% of patients are below the normal range for height. Height achieved post transplant is dependent on graft function and is better in younger children and those who have the best height attainment pre transplant. The use of steroid-free immunosuppressive regimens is encouraging. The prognosis for final height is improving.
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Carton, James. Renal pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0010.
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This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, reflux nephropathy, and obstructive nephropathy.
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Jayasumana, Channa, Carlos Orantes, and Marc E. De Broe. Chronic Interstitial Nephritis in Agricultural Communities. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0366_update_001.
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Chronic Interstitial Nephritis in Agricultural Communities (CINAC) has been increasingly recognized since the early 1990s. It has been called epidemic chronic kidney disease unknown cause (CKDu) in Sri Lanka, and meso-American nephropathy in Central America. CINAC occurs regionally in the Tropics, predominantly in rural/agricultural zones. It is increasingly recognized, but also believed to be increasing in incidence. Men are affected up to three times more often than women. Its incidence increases with age, and a number of other epidemiological factors impact on it. In some areas, such as the North Central Province of Sri Lanka and regions of Central America, it drives extreme rates of CKD and end-stage renal failure. Clinically, it has the non-specific characteristics of other slowly-evolving chronic interstitial nephritis (Chapter 86). Perhaps distinctive is an inconsistent history of episodes of dysuria, sometimes loin pain, in earlier disease. Its aetiology remains unsolved. Maps of incidence commonly show a mosaic pattern, suggesting that exposure to local factors are implicated. It has been associated with working outdoors in high temperatures, but this seems inadequate as the sole explanation. Exposure to nephrotoxins, natural or possibly as agrochemicals, seems likely.
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Speer, Thimoteus, and Danilo Fliser. Abnormal endothelial vasomotor and secretory function. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0113.
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The endothelium plays a crucial role in the maintenance of vascular integrity and function. Nitric oxide produced by endothelial cells is a key player, inducing relaxation of vascular smooth muscle cells, inhibition of vascular inflammation, and prevention of coagulatory activation. Chronic kidney disease (CKD) is characterized by deterioration of different protective endothelial properties, collectively described as endothelial dysfunction. Several factors such as methylarginines, modified lipoproteins, and other substances that accumulate may be involved in the pathogenesis of endothelial dysfunction of CKD. Endothelial dysfunction is suggested to be the first critical step in the initiation of atherosclerosis. Clinical assessment of endothelial function may become important in recognition of patients with increased cardiovascular risk. Beside several invasive and non-invasive methods to assess endothelial function in vivo, measurement of circulating (bio)markers may be useful for the evaluation of endothelial dysfunction.
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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.
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Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.
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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.