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Livros sobre o tema "Albuminurie"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 1 de fevereiro de 2022

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1

Winocour, Peter H. Microalbuminuria: Biochemistry, epidemiology and clinical practice. New York: Cambridge University Press, 1998.

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2

Cohen, Dianne. Human Serum Albumin: Structure, Binding and Activity. Nova Science Publishers, Incorporated, 2019.

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3

Awad, Alaa S., Nasrollah Ghahramani e Emaad M. Abdel-Rahman. Albuminuria: Symptoms, Causes and Treatment Options. Nova Science Publishers, Incorporated, 2013.

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4

On the functions of the glomeruli of the kidney: A contribution to the story of albuminuria. [S.l: s.n., 1985.

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5

On the functions of the glomeruli of the kidney: A contribution to the story of albuminuria. [S.l: s.n., 1985.

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6

Harley, George. Albuminuria, With And Without Dropsy: Its Different Forms, Pathology And Treatment. Kessinger Publishing, LLC, 2007.

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7

Erik, Mogensen Carl, ed. Microalbuminuria: A marker for end organ damage. 3^a ed. London: Science Press, 2004.

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8

Upadhyay, Ashish, Lesley A. Inker e Andrew S. Levey. Chronic kidney disease. Editado por 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.

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9

Monath, Thomas P., e J. Erin Staples. Yellow fever. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0045.

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Yellow fever is an acute mosquito-borne flavivirus infection characterized in its full-blown form by fever, jaundice, albuminuria, and haemorrhage. Two forms are distinguished: urban yellow fever in which the virus is spread from person to person by peridomestic Aedes aegypti mosquitoes and jungle (sylvan) yellow fever transmitted by tree-hole breeding mosquitoes between non-human primates and sometimes humans. Yellow fever is endemic and epidemic in tropical areas of the Americas and Africa but has never appeared in Asia or the Pacific region. Prevention and control are effected principally through yellow fever vaccination.

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10

Herrington, William G., Aron Chakera e Christopher A. O’Callaghan. Chronic kidney disease. Editado por Patrick Davey e 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.

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11

Schreuder, Michiel F. Renal agenesis. Editado por Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0346.

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In renal agenesis, the kidney never forms due to an absence of interaction in the developing embryo between the ureteric bud and the metanephric mesenchyme. Most cases of renal agenesis are unilateral, for which the reported incidence is around 1 in 3000. The prenatal diagnosis of unilateral renal agenesis is based on the absence of a recognizable kidney, either at the normal or an ectopic site. However, such cases of an empty renal fossa can also be explained by an involuted multicystic dysplastic kidney, or by renal aplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal agenesis is desirable.

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12

Johns Hopkins University. Use of Glycated Hemoglobin and Microabuminuria in the Monitoring of Diabetes Mellitus (Evidence Report/Technology Assessment). Agency for Healthcare Research and Quality, 2003.

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13

Use of glycated hemoglobin and microabuminuria in the monitoring of diabetes mellitus. [Rockville, Md.]: Agency for Healthcare Research and Quality, 2003.

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14

Levy, David. Macrovascular complications, hypertension, and lipids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0008.

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Premature vascular disease is common in Type 1 diabetes, especially in women and those with long duration. Many studies have identified early vascular involvement, using carotid Doppler and coronary artery calcification. Symptoms of coronary heart disease are often absent or muted, and the best methods for identifying occult coronary heart disease in Type 1 patients are not known. The concept of ideal cardiovascular health is valuable in planning preventive lifestyle and medical interventions. ‘Essential’ hypertension in young Type 1 patients is common, and reflects increased arterial stiffness. Hypertension is invariable in patients with any degree of albuminuria or renal impairment. Statin treatment in patients over 40 years old is recommended, but the evidence base is weak. Statins and ezetimibe are the only agents of prognostic value currently available for prevention of vascular events. Primary prevention with aspirin needs individual assessment. Insulin resistance/metabolic syndrome is frequent in Type 1 diabetes.

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15

Schreuder, Michiel F. Renal hypoplasia. Editado por Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0348.

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In true renal hypoplasia, normal nephrons are formed but with a deficit in total numbers. As nephron number estimation is not possible in vivo, renal size is used as a marker. A widely used definition of renal hypoplasia is kidneys with a normal appearance on ultrasound but with a size less than two standard deviations below the mean for gender, age, and body size. A distinct and severe form of renal hypoplasia is called (congenital) oligomeganephronia, which is characterized by small but normal-shaped kidneys with a marked reduction in nephron numbers (to as low as 10–20% of normal), a distinct enlargement of glomeruli, and a reduced renal function. In many cases, the small kidney also shows signs of dysplasia on ultrasound, leading to the diagnosis of renal hypodysplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal hypoplasia is desirable.

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16

Lopez, Berenice, e Patrick J. Twomey. Biochemical investigation of rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0062.

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It is important for rheumatologists to have an understanding of biochemical tests including an awareness of their limitations. The biological variability of an analyte both within and between individuals, the limitations of the measurement technology, the sensitivity of laboratory internal quality control and external quality assurance procedures, as well as interlaboratory variations in practices including sample collection procedures, may all impact on the interpretation of a result. Biochemical tests are often requested to monitor organ-specific dysfunction arising as an adverse consequence of pharmacotherapy or as a component of a systemic rheumatic disease, although dysfunction may also reflect infection or coincidental pathology. Patients with rheumatic diseases are at high risk of renal and hepatic disease. Serum creatinine and its derivative estimated glomerular filtration rate (eGFR) are the most readily available surrogate markers of GFR and are used to assess renal impairment and monitor its course. However, the use of creatinine alone lacks sensitivity and a substantial loss of function must occur before creatinine levels are increased. Additional biochemical screening for kidney damage can be performed by assessment of glomerular integrity, including proteinuria or albuminuria and haematuria. A wide spectrum of rheumatic diseases can affect the liver with various degrees of involvement and hepatic pathology. These often present with cholestatic or hepatitic biochemical profiles. The medical management of rheumatic diseases also involves medications that are hepatotoxic, and routine monitoring of liver function is recommended. This approach is not problem-free and may be improved by quantitative determinations of non-invasive markers of liver fibrosis in the future. Together with imaging techniques, biochemical tests play an important role in the assessment and differential diagnosis of metabolic bone disease.

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17

Haymann, Jean-Philippe, e Francois Lionnet. The patient with sickle cell anaemia. Editado por Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0167.

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In sickle cell anaemia (SCA) a single mutation in the haemoglobin beta-globin gene is responsible for a pleomorphic phenotype leading to acute and chronic life-threatening complications. Healthcare management programmes, patient and family education, infection prophylaxis (especially in childhood), and long-term treatment for some patients (such as hydroxyurea) have significantly improved survival, giving rise to some new long-term issues.Sickle cell-associated nephropathy (SCAN) leads in some cases to chronic renal failure with a significant impact on survival. SCAN is characterized by an increased effective plasma renal flow and glomerular filtration rate, glomerular hypertrophy, and damaged vasa recta system leading to albuminuria and impaired urinary concentration.Early onset of hyperfiltration occurs in 60% of SCA patients often associated with microalbuminuria. SCAN risk factors are still under investigation, but may be related to chronic haemolysis at an early time point. Other lesions in patients with sickle cell anaemia include papillary necrosis, and recurrent acute kidney injury in association with crises or infections.ACEI are recommended if there is proteinuria. There is no current agreement on whether angiotensin-converting enzyme inhibitors (ACEI) should be introduced earlier, but systematic screening for microalbuminuria and hypertension, and avoidance of nephrotoxic agents are strongly advised.Patients with sickle cell trait (carriers for sickle cell anaemia) are prone to microscopic haematuria and abnormalities of the vasa recta have been described. A very rare tumour, renal medullary carcinoma, is largely restricted to this group (in whom it is still extremely rare). Increased risk of other renal problems is still largely hypothetical rather than proven.The prevalence of nephropathies in other sickle cell diseases (in particular haemoglobin SC disease) is much lower.

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