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CESPE – FUB – Estatístico – 2015)O conceito médio da graduação (G) é um indicador calculado pelo INEP (Instituto Nacional de Estudos e Pesquisas Educacionais Anísio Teixeira) para a avaliação da qualidade dos cursos de graduação das instituições de ensino superior. A figura apresentada mostra, esquematicamente, as distribuições desse indicador nas instituições privadas e públicas, referentes ao ano de 2013, e a tabela apresenta algumas estatísticas descritivas referentes a essas distribuições.
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A kidney biopsy is often required to diagnose the underlying pathology in patients with suspected glomerular disease, particularly in those with nephrotic syndrome or suspected glomerulonephritis
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many inherited or acquired disorders and can manifest in a variety of ways, ranging in severity from asymptomatic urinary abnormalities to acute kidney injury (AKI) or end-stage kidney disease. <span>A kidney biopsy is often required to diagnose the underlying pathology in patients with suspected glomerular disease, particularly in those with nephrotic syndrome or suspected glomerulonephritis. Rarely, a biopsy cannot be performed or is not needed to secure a diagnosis. As examples: ●A biopsy may be deferred if the procedural risk is prohibitive or if the patient is uncoopera




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On a pathological basis, glomerular lesions can be diffuse (all glomeruli are involved) or focal (only some glomeruli are involved [typically less than 50 percent]). At the level of the individual glomerulus, a process is global if the whole glomerular tuft is involved or segmental if only a portion is involved (less than 50 percent)
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epithelial cells forming a cup-like sac that is continuous with the renal tubule, and into which the filtrate from the glomerular capillaries is collected and passed to the renal tubule [1,2]. <span>On a pathological basis, glomerular lesions can be diffuse (all glomeruli are involved) or focal (only some glomeruli are involved [typically less than 50 percent]). At the level of the individual glomerulus, a process is global if the whole glomerular tuft is involved or segmental if only a portion is involved (less than 50 percent). Histologic descriptions include the terms "proliferative" (an increase in the number of cells in the glomerulus), "sclerosing" (presence of scarring), and "necrotizing" (areas of cell




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Histologic descriptions include the terms "proliferative" (an increase in the number of cells in the glomerulus), "sclerosing" (presence of scarring), and "necrotizing" (areas of cell death). Proliferation may occur predominantly in the mesangium (mesangial proliferative glomerulonephritis), within the capillary wall (endocapillary hypercellularity), and in an extracapillary location. Extracapillary proliferation (also known as crescents) are lesions associated with accumulations of macrophages, fibroblasts, proliferating epithelial cells, and fibrin within Bowman's space and represent rupture of the glomerular membrane, signifying severe injury to the glomerular capillary wall
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ess than 50 percent]). At the level of the individual glomerulus, a process is global if the whole glomerular tuft is involved or segmental if only a portion is involved (less than 50 percent). <span>Histologic descriptions include the terms "proliferative" (an increase in the number of cells in the glomerulus), "sclerosing" (presence of scarring), and "necrotizing" (areas of cell death). Proliferation may occur predominantly in the mesangium (mesangial proliferative glomerulonephritis), within the capillary wall (endocapillary hypercellularity), and in an extracapillary location. Extracapillary proliferation (also known as crescents) are lesions associated with accumulations of macrophages, fibroblasts, proliferating epithelial cells, and fibrin within Bowman's space and represent rupture of the glomerular membrane, signifying severe injury to the glomerular capillary wall. Some examples of how this terminology is used include "focal and segmental necrotizing glomerulonephritis" and "diffuse global proliferative glomerulonephritis" (picture 2). Lastly, in




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Lastly, interstitial fibrosis, which accompanies uncontrolled glomerular disease, is a poor prognostic sign [3]
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lar capillary wall. Some examples of how this terminology is used include "focal and segmental necrotizing glomerulonephritis" and "diffuse global proliferative glomerulonephritis" (picture 2). <span>Lastly, interstitial fibrosis, which accompanies uncontrolled glomerular disease, is a poor prognostic sign [3]. Several mechanisms lead to glomerular dysfunction [2]. Podocyte dysfunction can occur in genetic disease, affecting key basement membrane proteins such as collagen IV mutations in Alpo




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Glomerular disease should be suspected when hematuria and/or proteinuria are seen on urinalysis. Glomerular hematuria is established by the presence of urinary red blood cell (RBC) casts (of any number) or hematuria in which a substantial proportion of RBCs are acanthocytes (picture 3)
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lomerular crescent formation".) CLINICAL MANIFESTATIONS OF GLOMERULAR DISEASE — Clinical manifestations associated with glomerular disease include the following: ●Hematuria and/or proteinuria – <span>Glomerular disease should be suspected when hematuria and/or proteinuria are seen on urinalysis. Glomerular hematuria is established by the presence of urinary red blood cell (RBC) casts (of any number) or hematuria in which a substantial proportion of RBCs are acanthocytes (picture 3). Although interstitial and vascular disorders of the kidney may also cause these abnormalities (and therefore mimic glomerular disease), the findings of dysmorphic RBCs and RBC casts in




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Patients with acute onset of nephrotic syndrome do not typically present with acute kidney injury (AKI). However, AKI may be seen at the time of presentation in patients with podocytopathies such as minimal change disease or primary focal segmental glomerulosclerosis (FSGS)
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ephrotic-range proteinuria (ie, more than 3 to 3.5 g/day of proteinuria) are more specific for a glomerular origin. (See "Urinalysis in the diagnosis of kidney disease".) ●Renal insufficiency – <span>Patients with acute onset of nephrotic syndrome do not typically present with acute kidney injury (AKI). However, AKI may be seen at the time of presentation in patients with podocytopathies such as minimal change disease or primary focal segmental glomerulosclerosis (FSGS). (See "Acute kidney injury (AKI) in minimal change disease and other forms of nephrotic syndrome".) However, renal impairment (acute or chronic) is commonly seen in patients with glomer




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However, renal impairment (acute or chronic) is commonly seen in patients with glomerulonephritis:

• AKI may occur with acute glomerulonephritis, especially in patients who have crescentic glomerulonephritis, which is often due to antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis or anti-glomerular basement membrane (GBM) disease.

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topathies such as minimal change disease or primary focal segmental glomerulosclerosis (FSGS). (See "Acute kidney injury (AKI) in minimal change disease and other forms of nephrotic syndrome".) <span>However, renal impairment (acute or chronic) is commonly seen in patients with glomerulonephritis: •AKI may occur with acute glomerulonephritis, especially in patients who have crescentic glomerulonephritis, which is often due to antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis or anti-glomerular basement membrane (GBM) disease. (See "Overview of the classification and treatment of rapidly progressive (crescentic) glomerulonephritis".) •Patients with chronic glomerular diseases may develop a progressive decline




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Acute onset of hypertension in someone with previously normal blood pressure or acute worsening of hypertension in someone with preexisting, controlled hypertension should raise suspicion for glomerular disease, particularly if other manifestations (eg, hematuria, edema) are also present
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ressive (crescentic) glomerulonephritis".) •Patients with chronic glomerular diseases may develop a progressive decline in glomerular filtration rate and chronic kidney disease. ●Hypertension – <span>Acute onset of hypertension in someone with previously normal blood pressure or acute worsening of hypertension in someone with preexisting, controlled hypertension should raise suspicion for glomerular disease, particularly if other manifestations (eg, hematuria, edema) are also present. ●Edema – The presence of peripheral and/or periorbital edema in patients with hematuria or proteinuria may be a sign of primary renal sodium retention as a result of glomerular disease




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The presence of peripheral and/or periorbital edema in patients with hematuria or proteinuria may be a sign of primary renal sodium retention as a result of glomerular disease
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ension in someone with preexisting, controlled hypertension should raise suspicion for glomerular disease, particularly if other manifestations (eg, hematuria, edema) are also present. ●Edema – <span>The presence of peripheral and/or periorbital edema in patients with hematuria or proteinuria may be a sign of primary renal sodium retention as a result of glomerular disease. ●Hypercoagulability – Some types of glomerular disease, in particular membranous nephropathy or, less commonly, other causes of nephrotic syndrome, may produce a hypercoagulable state.




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Some types of glomerular disease, in particular membranous nephropathy or, less commonly, other causes of nephrotic syndrome, may produce a hypercoagulable state. Thus, thrombotic events, such as pulmonary embolism, may be a manifestation of glomerular disease
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resence of peripheral and/or periorbital edema in patients with hematuria or proteinuria may be a sign of primary renal sodium retention as a result of glomerular disease. ●Hypercoagulability – <span>Some types of glomerular disease, in particular membranous nephropathy or, less commonly, other causes of nephrotic syndrome, may produce a hypercoagulable state. Thus, thrombotic events, such as pulmonary embolism, may be a manifestation of glomerular disease. ●Systemic findings – Glomerular disease may be limited primarily to the kidney or may be associated with systemic conditions such as infections, autoimmune disorders, malignancy, and d




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In the nephrotic syndrome, leakage of plasma proteins without inflammation is the primary pathogenic mechanism. Conversely, in glomerulonephritis, inflammation within the glomerulus leads not only to the passage of plasma proteins but also of inflammatory cells (leukocytes) and RBCs into the renal tubule. These classifications, however, are not exclusive, as some conditions may present with both patterns, and some disorders (eg, lupus nephritis) may progress from one pattern to the other.
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, the existence of systemic features, and the degree of kidney dysfunction (algorithm 1). The nephrotic syndrome and glomerulonephritis are the prototypical presentations of glomerular disease. <span>In the nephrotic syndrome, leakage of plasma proteins without inflammation is the primary pathogenic mechanism. Conversely, in glomerulonephritis, inflammation within the glomerulus leads not only to the passage of plasma proteins but also of inflammatory cells (leukocytes) and RBCs into the renal tubule. These classifications, however, are not exclusive, as some conditions may present with both patterns, and some disorders (eg, lupus nephritis) may progress from one pattern to the other. In addition, patients may present with mild manifestations such as isolated proteinuria or isolated hematuria. Proteinuria — Proteinuria may be caused by glomerular disease (in which th




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● Proteinuria due to glomerular disease (in which there is albuminuria) is identified on a urine dipstick or with a quantitative measurement of urine albumin excretion.

● Proteinuria that is not due to glomerular disease may be due to one of three mechanisms:

• Tubular proteinuria, in which low-molecular-weight proteins that are filtered across the glomerulus are incompletely reabsorbed by the renal tubule

• Overflow proteinuria, in which overproduction of low-molecular-weight proteins (eg, light chains in the patients with multiple myeloma) leads to an increase in filtration and excretion

• Postrenal proteinuria, which is typically associated with a urinary tract infection and leukocyturia

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e is albuminuria) or other disorders (table 1) (see "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Types of proteinuria'): <span>●Proteinuria due to glomerular disease (in which there is albuminuria) is identified on a urine dipstick or with a quantitative measurement of urine albumin excretion. ●Proteinuria that is not due to glomerular disease may be due to one of three mechanisms: •Tubular proteinuria, in which low-molecular-weight proteins that are filtered across the glomerulus are incompletely reabsorbed by the renal tubule •Overflow proteinuria, in which overproduction of low-molecular-weight proteins (eg, light chains in the patients with multiple myeloma) leads to an increase in filtration and excretion •Postrenal proteinuria, which is typically associated with a urinary tract infection and leukocyturia Proteinuria discovered by a semiquantitative urine dipstick typically reflects glomerular proteinuria because the dipstick is insensitive to nonalbumin proteins. However, if proteinuria




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Proteinuria discovered by a semiquantitative urine dipstick typically reflects glomerular proteinuria because the dipstick is insensitive to nonalbumin proteins. However, if proteinuria is discovered by a quantitative test for urinary protein (ie, a 24-hour urine collection or a random urine protein-to-creatinine ratio), the origin of the proteinuria can be determined with a dipstick, a quantification of urine albumin excretion (ie, a 24-hour urine collection or a random urine albumin-to-creatinine ratio), or with a urine protein electrophoresis and immunofixation
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ins in the patients with multiple myeloma) leads to an increase in filtration and excretion •Postrenal proteinuria, which is typically associated with a urinary tract infection and leukocyturia <span>Proteinuria discovered by a semiquantitative urine dipstick typically reflects glomerular proteinuria because the dipstick is insensitive to nonalbumin proteins. However, if proteinuria is discovered by a quantitative test for urinary protein (ie, a 24-hour urine collection or a random urine protein-to-creatinine ratio), the origin of the proteinuria can be determined with a dipstick, a quantification of urine albumin excretion (ie, a 24-hour urine collection or a random urine albumin-to-creatinine ratio), or with a urine protein electrophoresis and immunofixation. (See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Types of proteinuria'.) The evaluation and differential diagn




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The nephrotic syndrome is characterized by the following (see "Overview of heavy proteinuria and the nephrotic syndrome"):

● A urine protein excretion of greater than 3500 mg per 24 hours or, if a random urine protein-to-creatinine ratio is measured, a ratio greater than 3000 mg/g in an adult

● Hypoalbuminemia, usually less than 3.5 g/dL, depending on the method of measurement

Other common findings in patients with nephrotic syndrome include edema (peripheral or periorbital, occasionally ascites or pleural effusions), hyperlipidemia, and lipiduria

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erential diagnosis of patients with glomerular proteinuria depends, in part, upon whether or not the patient has nephrotic syndrome. Nephrotic syndrome (heavy proteinuria and hypoalbuminemia) — <span>The nephrotic syndrome is characterized by the following (see "Overview of heavy proteinuria and the nephrotic syndrome"): ●A urine protein excretion of greater than 3500 mg per 24 hours or, if a random urine protein-to-creatinine ratio is measured, a ratio greater than 3000 mg/g in an adult ●Hypoalbuminemia, usually less than 3.5 g/dL, depending on the method of measurement Other common findings in patients with nephrotic syndrome include edema (peripheral or periorbital, occasionally ascites or pleural effusions), hyperlipidemia, and lipiduria. Lipiduria is identified by the presence of fat droplets, which may be free within sloughed tubular cells (oval fat bodies) or inside fatty casts (picture 4). Fat droplets have a charac




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In addition to a kidney biopsy, certain laboratory tests, which are often performed in nephrotic patients, include:

● Glycated hemoglobin (HbA1C, to diagnose diabetes)

● Antinuclear antibody and anti-double stranded DNA (dsDNA) antibody

● Anti-PLA2R autoantibody

● In patients older than 50 years – Serum free light chains and serum protein immunofixation

● Tests for hepatitis B and C viruses and HIV (see "Hepatitis B virus: Screening and diagnosis", section on 'Diagnostic algorithms' and "Screening and diagnosis of chronic hepatitis C virus infection", section on 'Initial testing' and "Screening and diagnostic testing for HIV infection", section on 'Testing algorithm')

● Serum C3 and C4 complement levels

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see "Membranous nephropathy: Epidemiology, pathogenesis, and etiology") ●If a biopsy cannot be performed or is refused (eg, a patient in the later stages of pregnancy) (see "The kidney biopsy") <span>In addition to a kidney biopsy, certain laboratory tests, which are often performed in nephrotic patients, include: ●Glycated hemoglobin (HbA1C, to diagnose diabetes) ●Antinuclear antibody and anti-double stranded DNA (dsDNA) antibody ●Anti-PLA2R autoantibody ●In patients older than 50 years – Serum free light chains and serum protein immunofixation ●Tests for hepatitis B and C viruses and HIV (see "Hepatitis B virus: Screening and diagnosis", section on 'Diagnostic algorithms' and "Screening and diagnosis of chronic hepatitis C virus infection", section on 'Initial testing' and "Screening and diagnostic testing for HIV infection", section on 'Testing algorithm') ●Serum C3 and C4 complement levels Other serologic, microbiological, and genetic tests are sometimes performed in patients once a specific histologic diagnosis is established. Differential diagnosis of nephrotic syndrome




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The nephrotic syndrome may be primary (table 2) or secondary to a systemic disease (table 3). Secondary nephrotic syndrome due, for example, to diabetes, infection, or autoimmune disease, is more common than primary nephrotic syndrome. Overall, diabetic nephropathy is the most common cause of nephrotic syndrome.
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evels Other serologic, microbiological, and genetic tests are sometimes performed in patients once a specific histologic diagnosis is established. Differential diagnosis of nephrotic syndrome — <span>The nephrotic syndrome may be primary (table 2) or secondary to a systemic disease (table 3). Secondary nephrotic syndrome due, for example, to diabetes, infection, or autoimmune disease, is more common than primary nephrotic syndrome. Overall, diabetic nephropathy is the most common cause of nephrotic syndrome. (See "Overview of heavy proteinuria and the nephrotic syndrome", section on 'Etiology' and "Diabetic kidney disease: Pathogenesis and epidemiology".) Although minimal change disease is




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Although minimal change disease is the most common cause of primary nephrotic syndrome in children, membranous nephropathy and focal segmental glomerulosclerosis (FSGS) are the most common causes of primary nephrotic syndrome in adults. In adults, membranous nephropathy predominates in white patients and FSGS in black persons.
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he most common cause of nephrotic syndrome. (See "Overview of heavy proteinuria and the nephrotic syndrome", section on 'Etiology' and "Diabetic kidney disease: Pathogenesis and epidemiology".) <span>Although minimal change disease is the most common cause of primary nephrotic syndrome in children, membranous nephropathy and focal segmental glomerulosclerosis (FSGS) are the most common causes of primary nephrotic syndrome in adults. In adults, membranous nephropathy predominates in white patients and FSGS in black persons. (See "Membranous nephropathy: Epidemiology, pathogenesis, and etiology" and "Focal segmental glomerulosclerosis: Epidemiology, classification, clinical features, and diagnosis" and "Eti




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Some disorders (eg, C3 glomerulonephritis or other causes of a membranoproliferative pattern of injury) can present as nephrotic syndrome, glomerulonephritis, or both
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" and "Focal segmental glomerulosclerosis: Epidemiology, classification, clinical features, and diagnosis" and "Etiology, clinical features, and diagnosis of minimal change disease in adults".) <span>Some disorders (eg, C3 glomerulonephritis or other causes of a membranoproliferative pattern of injury) can present as nephrotic syndrome, glomerulonephritis, or both. (See "Overview of heavy proteinuria and the nephrotic syndrome".) Proteinuria without nephrotic syndrome — Glomerular proteinuria without nephrotic syndrome can range in severity from




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Glomerular proteinuria without nephrotic syndrome can range in severity from several hundred mg per day to the nephrotic range (ie, more than 3000 to 3500 mg per day). Such patients may also have variable degrees of renal insufficiency, hypertension, and hematuria. Glomerular proteinuria is said to be isolated when it occurs in the absence of systemic disease, hypertension, hematuria, or azotemia
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ive pattern of injury) can present as nephrotic syndrome, glomerulonephritis, or both. (See "Overview of heavy proteinuria and the nephrotic syndrome".) Proteinuria without nephrotic syndrome — <span>Glomerular proteinuria without nephrotic syndrome can range in severity from several hundred mg per day to the nephrotic range (ie, more than 3000 to 3500 mg per day). Such patients may also have variable degrees of renal insufficiency, hypertension, and hematuria. Glomerular proteinuria is said to be isolated when it occurs in the absence of systemic disease, hypertension, hematuria, or azotemia. The evaluation and differential diagnosis of proteinuria without nephrotic syndrome are presented below (algorithm 1). Evaluation of proteinuria without nephrotic syndrome — The evalua




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Orthostatic (also referred to as postural) proteinuria is characterized by an elevated protein excretion while in the upright position and normal protein excretion in a supine or recumbent position. It is the most frequent cause of isolated proteinuria in children, especially adolescents, and can be diagnosed by performing a split urine collection
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at they do not have kidney disease. (See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Rule out transient proteinuria'.) •<span>Orthostatic (also referred to as postural) proteinuria is characterized by an elevated protein excretion while in the upright position and normal protein excretion in a supine or recumbent position. It is the most frequent cause of isolated proteinuria in children, especially adolescents, and can be diagnosed by performing a split urine collection (table 4). Orthostatic proteinuria is discussed in detail elsewhere. (See "Orthostatic (postural) proteinuria" and "Assessment of urinary protein excretion and evaluation of isolated no




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Transient proteinuria is common, especially in young individuals. Transient proteinuria is diagnosed if a repeat qualitative test is no longer positive for proteinuria. These patients need no further evaluation and should be reassured that they do not have kidney disease.
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roteinuria and, if the patient is younger than 30 years, orthostatic proteinuria (see "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults"): •<span>Transient proteinuria is common, especially in young individuals. Transient proteinuria is diagnosed if a repeat qualitative test is no longer positive for proteinuria. These patients need no further evaluation and should be reassured that they do not have kidney disease. (See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Rule out transient proteinuria'.) •Orthostatic (also referred




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Patients who have isolated proteinuria that is persistent (ie, not transient and not orthostatic) should undergo kidney ultrasound to evaluate for structural disorders (eg, reflux nephropathy) and measurement of serum free light chains and a urine protein electrophoresis with immunofixation to evaluate for a monoclonal gammopathy
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Orthostatic (postural) proteinuria" and "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults", section on 'Rule out orthostatic proteinuria'.) <span>Patients who have isolated proteinuria that is persistent (ie, not transient and not orthostatic) should undergo kidney ultrasound to evaluate for structural disorders (eg, reflux nephropathy) and measurement of serum free light chains and a urine protein electrophoresis with immunofixation to evaluate for a monoclonal gammopathy. A kidney biopsy is seldom indicated for low levels of urinary protein (eg, less than 1 g per day). However, a biopsy may be helpful in patients with higher amounts of proteinuria. As a




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Rarely, a biopsy in subnephrotic patients may show findings suggestive of systemic disease (eg, amyloidosis, Fabry disease), which, if found, could lead to specific therapy.
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00 to 3500 mg per day) have shown membranous nephropathy, FSGS, infection-related glomerulonephritis, focal global sclerosis, mesangial proliferative glomerulonephritis, and normal kidneys [7]. <span>Rarely, a biopsy in subnephrotic patients may show findings suggestive of systemic disease (eg, amyloidosis, Fabry disease), which, if found, could lead to specific therapy. (See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults" and "Evaluation of proteinuria in children".) A kidney biopsy is usually in




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A kidney biopsy is usually indicated if a monoclonal gammopathy is present, if proteinuria is greater than 3000 to 3500 mg per day, or if the patient subsequently develops hematuria, azotemia, or a progressive increase in proteinuria.
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ound, could lead to specific therapy. (See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults" and "Evaluation of proteinuria in children".) <span>A kidney biopsy is usually indicated if a monoclonal gammopathy is present, if proteinuria is greater than 3000 to 3500 mg per day, or if the patient subsequently develops hematuria, azotemia, or a progressive increase in proteinuria. (See "Diagnosis and treatment of monoclonal gammopathy of renal significance", section on 'Diagnosis of MGRS' and "Assessment of urinary protein excretion and evaluation of isolated non




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Less common causes of glomerular proteinuria without nephrotic syndrome include early or mild membranous nephropathy, a mild form of glomerulonephritis (which may occasionally present without hematuria), or deposition disorders such as Fabry disease or amyloidosis.
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ephron mass, or to a prior inflammatory or other form of injury that resulted in fibrosis. (See "Focal segmental glomerulosclerosis: Pathogenesis", section on 'Pathogenesis of secondary FSGS'.) <span>Less common causes of glomerular proteinuria without nephrotic syndrome include early or mild membranous nephropathy, a mild form of glomerulonephritis (which may occasionally present without hematuria), or deposition disorders such as Fabry disease or amyloidosis. (See "Membranous nephropathy: Epidemiology, pathogenesis, and etiology" and "Fabry disease: Clinical features and diagnosis".) In addition, patients with no structural glomerular lesion




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The nephritic syndrome (ie, glomerulonephritis) is caused by glomerular inflammation that results in hematuria, variable degrees of proteinuria (which can sometimes be in the nephrotic range), and leukocyturia in the absence of urinary tract infection. Such patients may also have hypertension, renal insufficiency, and, if the inflammation is not limited to the kidney, findings that suggest involvement of other organ systems (eg, pulmonary hemorrhage, palpable purpura, arthritis)
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y contrast, glomerular hematuria may occur in isolation without any of these other abnormalities. Glomerulonephritis (hematuria with proteinuria, renal insufficiency, or other manifestations) — <span>The nephritic syndrome (ie, glomerulonephritis) is caused by glomerular inflammation that results in hematuria, variable degrees of proteinuria (which can sometimes be in the nephrotic range), and leukocyturia in the absence of urinary tract infection. Such patients may also have hypertension, renal insufficiency, and, if the inflammation is not limited to the kidney, findings that suggest involvement of other organ systems (eg, pulmonary hemorrhage, palpable purpura, arthritis). Glomerular inflammation is typically due to one of three major mechanisms (figure 2). (See 'Clinical manifestations of glomerular disease' above and "Mechanisms of immune injury of the




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Glomerulonephritis can present in a variety of ways, including a smoldering course characterized by a chronic, slowly progressive rise in serum creatinine and proteinuria (eventually leading to advanced chronic kidney disease and end-stage kidney disease), an acute, self-limited course, and a fulminant course with acute, progressive deterioration of kidney function. This last pattern is referred to as "rapidly progressive glomerulonephritis" and is typically associated with extensive crescents on the kidney biopsy.
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rular inflammation is typically due to one of three major mechanisms (figure 2). (See 'Clinical manifestations of glomerular disease' above and "Mechanisms of immune injury of the glomerulus".) <span>Glomerulonephritis can present in a variety of ways, including a smoldering course characterized by a chronic, slowly progressive rise in serum creatinine and proteinuria (eventually leading to advanced chronic kidney disease and end-stage kidney disease), an acute, self-limited course, and a fulminant course with acute, progressive deterioration of kidney function. This last pattern is referred to as "rapidly progressive glomerulonephritis" and is typically associated with extensive crescents on the kidney biopsy. (See "Overview of the classification and treatment of rapidly progressive (crescentic) glomerulonephritis".) The evaluation and differential diagnosis of suspected glomerulonephritis ar




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A kidney biopsy may be deferred in patients with advanced renal insufficiency who have small (likely fibrotic) kidneys by imaging since the diagnostic information gained is unlikely to have substantial benefit that outweighs the risks associated with kidney biopsy. Similarly, patients with normal kidney function, normal serological tests, and hematuria with low-grade proteinuria (<500 mg/day) may be observed without a biopsy since, even with a definitive diagnosis, it is unlikely that specific treatment will be instituted.
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rithm 1). Evaluation of glomerulonephritis — All patients with glomerulonephritis should be evaluated by a nephrologist and many should undergo a kidney biopsy to obtain a definitive diagnosis. <span>A kidney biopsy may be deferred in patients with advanced renal insufficiency who have small (likely fibrotic) kidneys by imaging since the diagnostic information gained is unlikely to have substantial benefit that outweighs the risks associated with kidney biopsy. Similarly, patients with normal kidney function, normal serological tests, and hematuria with low-grade proteinuria (<500 mg/day) may be observed without a biopsy since, even with a definitive diagnosis, it is unlikely that specific treatment will be instituted. (See "The kidney biopsy".) In addition to a kidney biopsy, certain laboratory tests should be obtained in patients with suspected glomerulonephritis, including: ●Serum C3 and C4 complem




#Glomérule #Glomérules #Néphrotique #Syndrome #UpToDate

In addition to a kidney biopsy, certain laboratory tests should be obtained in patients with suspected glomerulonephritis, including:

● Serum C3 and C4 complement levels

● Antineutrophil cytoplasmic autoantibodies (ANCA; using enzyme-linked immunosorbent assays [ELISAs] specific for proteinase-3 and myeloperoxidase)

● Anti-glomerular basement membrane (GBM) autoantibodies

● Antinuclear antibodies

● Anti-dsDNA antibodies

● Serology for hepatitis C virus, hepatitis B virus, and HIV

● Serum free light chains and serum immunofixation

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rade proteinuria (<500 mg/day) may be observed without a biopsy since, even with a definitive diagnosis, it is unlikely that specific treatment will be instituted. (See "The kidney biopsy".) <span>In addition to a kidney biopsy, certain laboratory tests should be obtained in patients with suspected glomerulonephritis, including: ●Serum C3 and C4 complement levels ●Antineutrophil cytoplasmic autoantibodies (ANCA; using enzyme-linked immunosorbent assays [ELISAs] specific for proteinase-3 and myeloperoxidase) ●Anti-glomerular basement membrane (GBM) autoantibodies ●Antinuclear antibodies ●Anti-dsDNA antibodies ●Serology for hepatitis C virus, hepatitis B virus, and HIV ●Serum free light chains and serum immunofixation In addition, some laboratory tests are indicated by the clinical context or biopsy findings. As examples: ●A cryocrit should be measured in patients with clinical features of cryoglobul




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In addition, some laboratory tests are indicated by the clinical context or biopsy findings. As examples:

● A cryocrit should be measured in patients with clinical features of cryoglobulinemia or a known history of hepatitis C virus infection.

● Blood cultures should be obtained in patients with persistent fever or other signs of chronic infection

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sement membrane (GBM) autoantibodies ●Antinuclear antibodies ●Anti-dsDNA antibodies ●Serology for hepatitis C virus, hepatitis B virus, and HIV ●Serum free light chains and serum immunofixation <span>In addition, some laboratory tests are indicated by the clinical context or biopsy findings. As examples: ●A cryocrit should be measured in patients with clinical features of cryoglobulinemia or a known history of hepatitis C virus infection. ●Blood cultures should be obtained in patients with persistent fever or other signs of chronic infection. Differential diagnosis of glomerulonephritis — Serum complement levels may be useful in differentiating the underlying etiology of glomerulonephritis; complement levels are typically n




#Glomérule #Glomérules #Néphrotique #Syndrome #UpToDate
Serum complement levels may be useful in differentiating the underlying etiology of glomerulonephritis; complement levels are typically normal in anti-GBM disease and pauci-immune glomerulonephritis but low in immune complex-mediated glomerulonephritis (with the exception of immunoglobulin A [IgA] nephropathy).
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history of hepatitis C virus infection. ●Blood cultures should be obtained in patients with persistent fever or other signs of chronic infection. Differential diagnosis of glomerulonephritis — <span>Serum complement levels may be useful in differentiating the underlying etiology of glomerulonephritis; complement levels are typically normal in anti-GBM disease and pauci-immune glomerulonephritis but low in immune complex-mediated glomerulonephritis (with the exception of immunoglobulin A [IgA] nephropathy). However, in practice, a kidney biopsy is almost always required to secure the diagnosis. In patients with an acute presentation of microangiopathic hemolytic anemia, thrombocytopenia, a




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However, patients with subacute and chronic TMA may exhibit minimal or no hematological or systemic abnormalities but present with progressive kidney failure with or without proteinuria and hematuria (eg, in drug-induced TMA) [8,9]. Such patients do need to be biopsied to secure the diagnosis.
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emia, thrombocytopenia, and kidney failure, the diagnosis of thrombotic microangiopathy (TMA) is a clinical one, and such patients typically do not need a kidney biopsy to secure the diagnosis. <span>However, patients with subacute and chronic TMA may exhibit minimal or no hematological or systemic abnormalities but present with progressive kidney failure with or without proteinuria and hematuria (eg, in drug-induced TMA) [8,9]. Such patients do need to be biopsied to secure the diagnosis. (See "Approach to the patient with suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".) Certain clinical findings suggest specific etiologies of glomerulonephritis: ●Gross h




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Gross hematuria may sometimes accompany glomerulonephritis and be associated with upper respiratory infection. The time elapsed between the respiratory infection and the appearance of hematuria may sometimes be helpful: If a latent period of 7 to 10 days occurs between the onset of infection and gross hematuria, poststreptococcal glomerulonephritis (especially in children) is the usual culprit. Hematuria occurring concurrently with the onset of infection (ie, "synpharyngitic glomerulonephritis") is typical of IgA nephropathy
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the diagnosis. (See "Approach to the patient with suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".) Certain clinical findings suggest specific etiologies of glomerulonephritis: ●<span>Gross hematuria may sometimes accompany glomerulonephritis and be associated with upper respiratory infection. The time elapsed between the respiratory infection and the appearance of hematuria may sometimes be helpful: If a latent period of 7 to 10 days occurs between the onset of infection and gross hematuria, poststreptococcal glomerulonephritis (especially in children) is the usual culprit. Hematuria occurring concurrently with the onset of infection (ie, "synpharyngitic glomerulonephritis") is typical of IgA nephropathy. ●The presence of palpable purpura or a petechial rash suggest an underlying vasculitis (eg, ANCA-associated vasculitis, IgA vasculitis [Henoch-Schönlein purpura], or cryoglobulinemia).




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The presence of palpable purpura or a petechial rash suggest an underlying vasculitis (eg, ANCA-associated vasculitis, IgA vasculitis [Henoch-Schönlein purpura], or cryoglobulinemia). Rarely, lupus nephritis may be associated with vasculitis.
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lonephritis (especially in children) is the usual culprit. Hematuria occurring concurrently with the onset of infection (ie, "synpharyngitic glomerulonephritis") is typical of IgA nephropathy. ●<span>The presence of palpable purpura or a petechial rash suggest an underlying vasculitis (eg, ANCA-associated vasculitis, IgA vasculitis [Henoch-Schönlein purpura], or cryoglobulinemia). Rarely, lupus nephritis may be associated with vasculitis. (See "Overview of cutaneous small vessel vasculitis".) ●The presence of pulmonary hemorrhage ("pulmonary renal syndrome") also suggests an underlying vasculitis. (See "The diffuse alveo




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The presence of pulmonary hemorrhage ("pulmonary renal syndrome") also suggests an underlying vasculitis.
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d vasculitis, IgA vasculitis [Henoch-Schönlein purpura], or cryoglobulinemia). Rarely, lupus nephritis may be associated with vasculitis. (See "Overview of cutaneous small vessel vasculitis".) ●<span>The presence of pulmonary hemorrhage ("pulmonary renal syndrome") also suggests an underlying vasculitis. (See "The diffuse alveolar hemorrhage syndromes".) Isolated glomerular hematuria — Persistent glomerular hematuria is distinguished from transient hematuria by repeating the urinalysis




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Persistent glomerular hematuria is distinguished from transient hematuria by repeating the urinalysis over a period of weeks to months. Transient hematuria is a relatively common finding over time in adults and may be induced by factors such as exercise or infection.
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".) ●The presence of pulmonary hemorrhage ("pulmonary renal syndrome") also suggests an underlying vasculitis. (See "The diffuse alveolar hemorrhage syndromes".) Isolated glomerular hematuria — <span>Persistent glomerular hematuria is distinguished from transient hematuria by repeating the urinalysis over a period of weeks to months. Transient hematuria is a relatively common finding over time in adults and may be induced by factors such as exercise or infection. (See "Isolated and persistent glomerular hematuria in adults" and "Etiology and evaluation of hematuria in adults" and "Exercise-induced hematuria".) Persistent glomerular hematuria is




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Generally, patients with isolated glomerular hematuria are likely to have mild IgA nephropathy, a disorder associated with membranoproliferative glomerulonephritis, a genetic mutation in type IV collagen associated with Alport syndrome, or thin basement membrane nephropathy.
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gnosis, and treatment of Alport syndrome (hereditary nephritis)" and "Thin basement membrane nephropathy (benign familial hematuria)".) Differential diagnosis of isolated glomerular hematuria — <span>Generally, patients with isolated glomerular hematuria are likely to have mild IgA nephropathy, a disorder associated with membranoproliferative glomerulonephritis, a genetic mutation in type IV collagen associated with Alport syndrome, or thin basement membrane nephropathy. (See "Isolated and persistent glomerular hematuria in adults" and "Clinical presentation and diagnosis of IgA nephropathy" and "Genetics, pathogenesis, and pathology of Alport syndrome




Flashcard 6248133954828

Question
[T] to choose someone for a job or position
Answer
appoint v.

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Flashcard 6248135789836

Question

1 [C] an arrangement to meet someone at a particular time and place

2 [C, U] when someone is chosen to do a job, or the job itself

Answer
appointment n.

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Flashcard 6248137624844

Question
a political and economic group of countries formed in 1967 which now has 10 members, including Indonesia, Malaysia, the Philippines, Singapore, Thailand and Vietnam
Answer
Association of South-East Asian Nations (ASEAN n.)

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Flashcard 6248139459852

Question
[C] something belonging to an individual or a business that has value or the power to earn money
Answer
asset n.

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Flashcard 6248141294860

Question

1 [C] a piece of work that someone is given

2 [U] when someone is given a particular job or task, or sent to work in a particular place or for a particular person

Answer
assignment n.

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Flashcard 6248143129868

Question

1 someone who you work with or do business with

2 a member of an organisation who has some but not all the rights of a full member

Answer
associate n. [C]

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Flashcard 6248144964876

Question
to go to an event, such as a meeting
Answer
attend v. [I, T]

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Flashcard 6248146799884

Question
an official organisation which controls a particular activity and checks that the rules and laws relating to it are being obeyed
Answer
authority n. ( plural authorities) 1 [C]

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Flashcard 6248148634892

Question
a government organisation in Britain that is responsible for providing public services, such as schools, the collection of rubbish, etc. in a particular area
Answer
local authority [C]

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Flashcard 6248150469900

Question
the organisations that are in charge of a particular country or area or a particular activity
Answer
the authorities [plural]

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Flashcard 6248152304908

Question
the power that a person or organisation has because of their official or legal position
Answer
authority

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Flashcard 6248154139916

Question
to give official or legal permission for something authorised ( also authorized AmE ) adj.
Answer
authorise ( also authorize AmE ) v. [T]

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Flashcard 6248155974924

Question
[only before a noun] relating to cars or the car industry
Answer
automotive adj.

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Flashcard 6248157809932

Question
knowledge or understanding of a particular subject, situation or thing
Answer
awareness n. [U]

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Flashcard 6248159644940

Question
an amount of money that is given to someone as a result of an official decision or judgement
Answer
award n. [C] 1

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Flashcard 6248161479948

Question
something such as a prize or an amount of money given to a person or company to reward them for something they have done
Answer
award 1 n. [C] 2

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Flashcard 6248163314956

Question
to officially decide that someone should have something, such as an amount of money
Answer
award v. [T] 1

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Flashcard 6248165149964

Question
to officially give a prize or an amount of money to a person or company, to reward them for what they have done
Answer
award 2 v. [T] 2

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Flashcard 6248167771404

Question
someone’s past, for example their education, qualifications, and the jobs they have had
Answer
background n. 1 [C]

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Flashcard 6248169606412

Question
the situation or past events that explain why something happens in the way that it does [+ to ]
Answer
background n. 2 [C, U]

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Flashcard 6248171441420

Question
not having enough money to pay your debts
Answer
bankrupt adj.

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Flashcard 6248173276428

Question
when someone is judged to be unable to pay their debts by a court of law, and their assets are shared among the people and businesses that they owe money to
Answer
bankruptcy n. ( plural bankruptcies) [C, U]

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Flashcard 6248175111436

Question
an advertisement that appears across the top of a page on the Internet
Answer
banner ad n. [C]; banner advertising n. [U]

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Flashcard 6248179830028

Question
something that makes trade between two countries more difficult or expensive, for example a tax on imports
Answer
barrier to trade n. ( plural barriers to trade) [C] (= trade barrier)

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Flashcard 6248181665036

Question
an offer to buy something, for example a company in a takeover; the price offered
Answer
bid n. [C]

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Flashcard 6248183500044

Question
a list showing how much you have to pay for services or goods received
Answer
bill 1 n. [C] 1 (= invoice)

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Flashcard 6248185335052

Question
a list showing how much you have to pay for food you have eaten in a restaurant
Answer
bill n. [C] 2 BrE (= check AmE )

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Flashcard 6248187956492

Question
send a bill to someone saying how much they owe
Answer
bill v. [T] (= invoice)

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Flashcard 6248189791500

Question
a large sign used for advertising
Answer
billboard n. [C] (= hoarding BrE )

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Flashcard 6248191626508

Question
the group of people who have been elected to manage a company by those holding shares in the company
Answer
board n. [C] ( also board of directors)

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Flashcard 6248193461516

Question
the place in a company where its board of directors meets
Answer
boardroom n. [C]

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Flashcard 6248195296524

Question
an extra amount of money added to an employee’s wages, usually as a reward for doing difficult work or for doing their work well
Answer
bonus n. [C]

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Flashcard 6248197131532

Question
an arrangement in which a place on a plane, in a hotel, restaurant, etc. is kept for a customer who will arrive later (= reservation
Answer
booking n. [C]

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Flashcard 6248198966540

Question
to increase something such as production, sales or prices
Answer
boost v. [T]

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Flashcard 6248200801548

Question
the figure showing a company’s total profit or loss
Answer
bottom line n. [C] informal 1

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Flashcard 6248202636556

Question
the end result of something or the most important point about something
Answer
bottom line n. [C] informal 2

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Flashcard 6248204471564

Question
an individual bank, shop, office, etc. that is part of a large organisation
Answer
branch n. [C]

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