CHAPTER 8: RENAL DISEASE Flashcards

1
Q

Deposition of immune complexes, in conjunction with streptococcal Infection, on the glomerular membrane

A

Acute or Post-streptococcal
Glomerulonephritis

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2
Q

Deposition of immune complexes from systemic immune disorders on the glomerular membrane

A

Rapidly Progressive Glomerulonephritis

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3
Q

Attachment of a cytotoxic antibody formed during viral respiratory infections to glomerular and alveolar
basement membranes

A

Goodpasture’s Syndrome

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4
Q

Binding of antineutrophilic cytoplasmic antibody to neutrophils in vessel walls

A

Wegener’s Granulomatosis

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5
Q

Disruption of vascular integrity
following viral respiratory infections

A

Henoch-Schonlein Purpura

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6
Q

Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA

A

IgA Nephropathy

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7
Q

Thickening of the glomerular membrane following IgG immune complex deposition associated with systemic disorders

A

Membranous Glomerulonephritis (MGN)

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8
Q

Type of MPGN that displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman capsule), causing thickening of the capillary walls

A

Type 1 Membranoproliferative glomerulonephritis (MPGN)

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9
Q

Type of MPGN that displays extremely dense deposits in the glomerular basement membrane, tubules, and Bowman capsule

A

Type 2 Membranoproliferative glomerulonephritis (MPGN)

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10
Q

Type of MPGN that is characterized by both subepithelial and subendothelial deposits

A

Type 3 Membranoproliferative glomerulonephritis (MPGN)

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11
Q

Refers to a sterile, inflammatory process that affects the glomerulus and is associated with the finding of blood, protein, and casts in the urine

A

Glomerulonephritis

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12
Q

Marked by the sudden onset of symptoms consistent with damage to the glomerular membrane

A

Acute glomerulonephritis (AGN)

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13
Q

Symptoms usually occur in children and young adults after respiratory infections caused by certain strains of group A β-hemolytic streptococci that contain M protein in the cell wall

A

Acute glomerulonephritis (AGN)

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14
Q

Primary urinalysis findings include marked hematuria, proteinuria, and oliguria, accompanied by red blood cell (RBC) casts, dysmorphic RBCs, hyaline and granular casts, and white blood cells (WBCs)

A

Acute glomerulonephritis (AGN)

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15
Q

These are a hallmark characteristic of acute glomerulonephritis

A

RBC casts

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16
Q

Formerly called Wegener granulomatosis

A

Granulomatosis with polyangiitis (GPA)

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16
Q

This autoantibody can be detected in a patient’s serum

A

Antiglomerular basement membrane antibody

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17
Q

Initial laboratory results are similar to AGN but become
more abnormal as the disease progresses, including protein levels that are markedly elevated and glomerular filtration rates
that are very low

A

Rapidly Progressive (or crescentic) Glomerulonephritis (RPGN)

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18
Q

Key to the diagnosis of GPA is the
demonstration of?

A

Antineutrophilic cytoplasmic antibody (ANCA) in the patient’s serum

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19
Q

If the neutrophils are fixed in ethanol, the antibodies form a perinuclear pattern which is called?

A

p-ANCA

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19
Q

This includes incubating the patient’s serum with either ethanol or formalin/formaldehyde-fixed neutrophils and examining the preparation using indirect immunofixation to detect the serum antibodies attached to the neutrophils

A

ANCA for GPA

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20
Q

This disease occurs primarily in children after upper respiratory infections.

A

Henoch-Schönlein Purpura

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20
Q

When the neutrophils are fixed with formalin/formaldehyde, the pattern is granular
throughout the cytoplasm
and is referred to as

A

c-ANCA

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21
Q

Cellular proliferation affecting the capillary walls or the glomerular basement membrane

A

Membranoproliferative Glomerulonephritis

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22
Q

A marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders

A

Chronic Glomerulonephritis

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23
Q

Disruption of the electrical charges that produce the tightly fitting podocyte barrier resulting in a massive loss of protein and lipids

A

Nephrotic Syndrome

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24
Q

Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and with HIV and hepatitis viruses

A

Focal Segmental Glomerulosclerosis

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25
Q

Disruption of the podocytes that occurs primarily in children after allergic reactions and immunizations; dysfunction of T-cell immunity

A

Minimal Change Disease (MCD)

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26
Q

Ascending bacterial infection of the bladder

A

Cystitis

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27
Q

Complete recovery with normal renal function is seen in more than 50% of patients.

In other patients, progression to a more serious form of glomerulonephritis and renal failure may occur

A

Henoch-Schönlein Purpura

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28
Q

Its predominant characteristic is a pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes

A

Membranous Glomerulonephritis

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29
Q

Their presence is often seen in chronic glomerulonephritis that progresses to ESRD

A

Broad casts

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30
Q

Also known as Berger disease

A

IgA nephropathy

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31
Q

The most common cause of glomerulonephritis.

A

IgA nephropathy

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32
Q

Marked by massive proteinuria (greater than 3.5 g/day), low levels of serum albumin, high levels of serum lipids, and pronounced edema

A

Nephrotic syndrome

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33
Q

Genetic disorder showing lamellated and thinning glomerular basement membrane

A

Alport syndrome

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33
Q

Acute onset after systemic shock

Gradual progression from other glomerular disorders and then to renal failure

A

Nephrotic syndrome (NS)

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33
Q

Frequent complete remission after corticosteroid treatment

A

Minimal change disease (MCD)

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33
Q

It may resemble nephrotic syndrome (NS) or minimal change disease (MCD)

A

Focal segmental glomerulosclerosis (FSGS)

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33
Q

Slow progression to nephrotic syndrome (NS) and end-stage renal disease

A

Alport syndrome

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33
Q

Hemoptysis and dyspnea followed by hematuria

A

Goodpasture syndrome

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33
Q

Their presence in the urine sediment is characteristic
for ATN

A

RTE cell casts and RTE cells

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33
Q

Demonstration of positive results of these tests provides evidence that the disease is of streptococcal origin (2pts)

A

Anti–group A streptococcal enzyme tests (antistreptolysin O [ASO] and
Antideoxyribonuclease-B antibody [anti-DNase B])

These are under the Acute Poststreptococcal Glomerulonephritis

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33
Q

This may be elevated during the acute stages of AGN, but, like the urinalysis, returns to normal

A

Blood Urea Nitrogen (BUN)

33
Q

Since the development of this, which can be performed in a physician’s office, urgent care facility, or emergency department, the incidence of acute poststreptococcal glomerulonephritis has declined.

A

rapid anti–group A streptococcal
enzyme tests

33
Q

Secondary complications of AGN

A

Hypertension and Electrolyte imbalance

33
Q

Morphological changes to the glomeruli resembling those in rapidly progressive glomerular nephritis are seen in conjunction with?

A

the autoimmune disorder termed Goodpasture syndrome

34
Q

Initial pulmonary complaints are hemoptysis and dyspnea, followed by the development of hematuria

A

Goodpasture syndrome

34
Q

Urinalysis results include proteinuria, hematuria, and the presence of RBC casts.
Progression to chronic glomerulonephritis and end-stage renal failure is common

A

Goodpasture syndrome

34
Q

Initial symptoms include the appearance of raised, red patches on the skin

A

Henoch-Schönlein purpura

34
Q

Causes a granuloma-producing inflammation of the small blood vessels, primarily of the kidney
and respiratory system

A

Granulomatosis with polyangiitis (GPA)

34
Q

Renal involvement is the most serious complication of this disorder and may range from mild to heavy proteinuria and hematuria with RBC casts

A

Henoch-Schönlein Purpura

34
Q

Respiratory and gastrointestinal symptoms, including blood in the sputum and stools, may be present

A

Henoch-Schönlein Purpura

35
Q

Disorders associated with the development of this disease include SLE, Sjögren syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, and malignancy.

A

Membranous Glomerulonephritis (MGN)

36
Q

In MGN, about 75% of cases,
the etiology is?

A

Unknown

37
Q

This disease has a tendency
toward thrombosis.

A

Membranous Glomerulonephritis (MGN)

38
Q

Laboratory findings include microscopic hematuria and elevated urine protein excretion that may reach concentrations similar to those in nephrotic syndrome. RBC casts are rare, but microscopic hematuria is common

A

Membranous Glomerulonephritis (MGN)

39
Q

In MPGN, Type 1 patients progress to?

While Type 2 patients experience symptoms of?

A

Type 1: Nephrotic syndrome
Type 2: Chronic glomerulonephritis

40
Q

Progression of glomerulonephritis from one form to another:

A

Rapidly progressive glomerulonephritis > chronic glomerulonephritis > nephrotic syndrome > renal failure

41
Q

There is a high incidence of recurrence of this disease after renal transplant

A

Membranoproliferative glomerulonephritis (MPGN)

41
Q

Its laboratory findings vary, but hematuria, proteinuria, and decreased serum complement levels are usual findings. There appears to be an association with autoimmune disorders, infections, and malignancies.

A

Membranoproliferative glomerulonephritis (MPGN)

42
Q

Except for periodic episodes of macroscopic hematuria, a patient with this disorder may remain essentially asymptomatic for 20 years or more; however, there is a gradual progression to chronic glomerulonephritis and ESRD

A

IgA nephropathy

43
Q

A glomerular filtration rate that is markedly decreased is present in conjunction with increased BUN and creatinine levels and electrolyte imbalance

A

Chronic Glomerulonephritis (CGN)

43
Q

Primary urinary results in the early stages of IgA nephropathy

A

Macroscopic or microscopic
hematuria

44
Q

Primary urinary results in the late stages of IgA nephropathy

A

Chronic glomerulonephritis (CGN)

44
Q

Damage to renal tubular cells caused by ischemia or toxic age

A

Acute tubular necrosis (ATN)

45
Q

Acute onset of renal dysfunction usually resolved when underlying cause is corrected

A

Acute tubular necrosis (ATN)

46
Q

Inherited in association with cystinosis and Hartnup disease or acquired through exposure to toxic agents

A

Fanconi syndrome

47
Q

Generalized defect in renal tubular reabsorption requiring supportive therapy

A

Fanconi syndrome

48
Q

Inherited defect in the production of normal uromodulin by the renal tubules and increased uric acid causing gout

A

Uromodulin-associated
kidney disease

49
Q

Continual monitoring of renal function for progression to renal failure and possible kidney transplantation

A

Uromodulin-associated
kidney disease

50
Q

Inherited defect of tubular response to ADH or
acquired from medications

A

Nephrogenic diabetes insipidus (DI)

50
Q

Requires supportive therapy to prevent dehydration

A

Nephrogenic diabetes insipidus (DI)

51
Q

Benign disorder

A

Renal glucosuria

51
Q

Inherited autosomal recessive trait

A

Renal glucosuria

52
Q

Acute onset of urinary frequency and burning; resolved with antibiotics

A

Cystitis

53
Q

Infection of the renal tubules and interstitium related to interference of urine flow to the bladder, reflux of urine from the bladder, and untreated cystitis

A

Acute pyelonephritis

54
Q

Recurrent infection of the renal tubules and interstitium caused by structural abnormalities affecting the flow of urine

A

Chronic pyelonephritis

55
Q

Acute onset of urinary frequency, burning, and lower back pain; resolved with antibiotics

A

Acute pyelonephritis

56
Q

Frequently diagnosed in children; requires correction of the underlying structural defect

Possible progression to renal failure

A

Chronic pyelonephritis

57
Q

Allergic inflammation of the renal interstitium in response to certain medications

A

Acute interstitial nephritis (AIN)

58
Q

Acute onset of renal dysfunction often accompanied by a skin rash

Resolves after discontinuation of medication and treatment with corticosteroids

A

Acute interstitial nephritis (AIN)

59
Q

Renal calculi (kidney stones) may form in the:

A
  • calyces and pelvis of the kidney
  • ureters
  • bladder
60
Q

In this condition, the calculi vary in size from barely visible to large, staghorn calculi resembling the shape of the renal pelvis and smooth, round bladder stones with diameters of 2 or more inches.

A

Renal Lithiasis

61
Q

Conditions favoring the formation of renal calculi are similar to those favoring the formation of urinary crystals, including:

A
  • pH
  • chemical concentration
  • urinary casts
62
Q

Broad casts are often referred to as?

A

Renal failure casts

63
Q

A procedure using high-energy shock waves, can be used to break stones located in the upper urinary tract into pieces that then can be passed in the urine.

A

Lithotripsy

64
Q

This has little importance
in predicting calculi formation

A

crystals

64
Q

This has been noted during the summer months in people known to form renal calculi

A

Increased crystalluria

65
Q

Approximately 75% of the renal calculi are composed of?

A

calcium oxalate or calcium phosphate

66
Q

These are the other primary
calculi constituent

A
  • Ammonium magnesium phosphate (struvite/ triple phosphate)
  • Uric acid
  • cystine
67
Q

Frequently this is associated with metabolic calcium and phosphate disorders and, occasionally, diet

A

calcium calculi

68
Q

May be associated with an increased intake of foods with high purine content and uromodulin-associated kidney disease.

A

Uric acid

69
Q

Identify if pre, renal, or postrenal causes of ARF:
- Acute glomerulonephritis (AGN)
- Acute tubular necrosis (ATN)
- Acute pyelonephritis
- Acute interstitial nephritis (AIN)

A

Renal

70
Q

Identify if pre, renal, or postrenal causes of ARF:
- Renal calculi
- Tumors

A

Postrenal

71
Q

Identify if pre, renal, or postrenal causes of ARF:
- Decreased blood pressure/cardiac output
- Hemorrhage
- Burns
- Surgery
- Septicemia

A

Prerenal

72
Q

It exists in both acute and chronic forms.

A

Renal failure

72
Q

In contrast to chronic renal failure, this exhibits a sudden loss of renal function and frequently is reversible

A

Acute Renal Failure (ARF)

73
Q

Renal calculi is also known as?

A

Kidney stones

74
Q

Its urinalysis findings include glycosuria with normal blood glucose and possible mild proteinuria.

Urinary pH can be very low due to the failure to reabsorb bicarbonate

A

Fanconi syndrome

75
Q

The disorder associated with tubular dysfunction most frequently is?

A

Fanconi syndrome

76
Q

The syndrome can be inherited as a sex-linked or autosomal genetic disorder.

Males inheriting the X-linked gene are affected more severely than females inheriting the autosomal gene.

A

Alport Syndrome

77
Q

Can be inherited as a sex-linked recessive gene or acquired from medications, including lithium and amphotericin B. It also may be seen as a complication of polycystic kidney disease and sickle cell anemia.

A

Nephrogenic DI

78
Q

This affects only the reabsorption of glucose

A

Renal Glycosuria

79
Q

This is significant for differentiating between cystitis and pyelonephritis.

A

WBC casts

80
Q

Their presence in the urine sediment is characteristic for AIN

A

Eosinophil casts and eosinophils

81
Q

General characteristics of ARF:

A

decreased glomerular filtration rate, oliguria, edema, and azotemia.

82
Q

Provides a more comprehensive analysis of Renal Lithiasis

A

X-ray crystallography