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CPR II Exam #2 > Renal Pathology I > Flashcards

Renal Pathology I Flashcards

1
Q

The 2 most common causes of CRF/ERSD are…

A
  1. DM

2. HTN

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2
Q

Prototypical disease process of glomeruli is…

A

Glomerulonephritis

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3
Q

Prototypical disease process of tubules is…

A

Bence-Jones proteinuria

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4
Q

Prototypical disease process of interstitium is…

A

Fibrosis, inflammation or edema

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5
Q

Prototypical disease process of renal vessels is…

A

Vasculitis, nephrosclerosis

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6
Q

Definition of Azotemia

A

Biochemical abnormality resulting in elevated BUN and creatinine and is usually associated with decreased GFR

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7
Q

Azotemia is usually a result of renal disorders, but it can also be from pre-renal azotemia and post-renal azotemia, which are…

A

Pre-renal: occurs after hypoperfusion of kidneys (clood loss, CHF, etc.) and impairs renal function without damage to the renal parenchyma.

Post-renal: seen when whenever urine flow is obstructed. Removing the obstruction will relieve the azotemia.

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8
Q

Definition of Uremia

A

Azotemia in addition to clinical findings and biochemical abnormalities resulting from renal damage.

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9
Q

What makes a diagnosis of uremia difficult in kids?

A

The SX are often nonspecific and can become chronic and progressive due to gradual onset of disease.

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10
Q

What metabolic abnormalities may result from uremia?

A

Anemia
Acidemia
Electrolyte abnormalities

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11
Q

What happens to glycemic control for diabetics as renal function declines?

A

It improves generally, but they may have more hypoglycemic episodes. This is due to increased insulin secretion and prolongation of its half-life.

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12
Q

Fluid/electrolyte manifestations of uremia

A

Dehydration
Edema
Hyperkalemia
Metabolic acidosis

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13
Q

Ca++ and PO4- manifestations of uremia

A

Hyperphosphatemia

Hypocalcemia

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14
Q

Hematologic manifestations of uremia

A

Anemia

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15
Q

Cardiopulmonary manifestations of uremia

A 
HTN
CHF
CM
Pulmonary edema
Pericarditis
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16
Q

GI manifestations of uremia

A

N/V

GI inflammation

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17
Q

Neuromuscular manifestations of uremia

A

Myopathy
Peripheral neuropathy
Encephalopathy

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18
Q

Derm manifestations of uremia

A

Pruritis

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19
Q

Normal GFR

A

Approx. 100 mL/min

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20
Q

Acute kidney injury (AKI)

Effects on GFR:

Urine production?

What causes it?

What is the progression?

A

Rapid decline in GFR

Severe forms show oliguria or anuria

May result from glomerular, interstitial, vascular or acute tubular injury

Can be reversible, or may progress to CKD

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21
Q

Chronic kidney disease (CKD)

Mild vs. severe forms:

How is it diagnosed?

What is the progression?

A

Mild - clinically silent, Severe - uremia

Persistent diminished GFR < 60 mL/min for at least 3 mo. OR persistent albuminemia

CKD is generally irreversible

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22
Q

End-stage renal disease (ESRD)

Effects on GFR:

It is the end-stage of…

A

GFR < 5% of normal

End stage of uremia

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23
Q

Which diseases/problems are primarily renal interstitial disease?

A

UTI
UT obstruction
Renal tumors
Nephrolithiasis

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24
Q

Definition of nephrotic syndrome

A

Glomerular disease characterized by:

Severe proteinuria (more than 3.5 gm/day)

Hypoalbuminemia (<3 gm/dL)

Severe edema

Hyperlipidemia

Lipiduria

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25
Q

What is the mechanism for the hyperlipidemia seen in nephrotic syndrome?

A

It is a compensatory mechanism from the liver in an effort to increase oncotic pressure, which was reduced due to the proteinuria. Fat can build up in the kidneys as well.

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26
Q

Definition of nephritic syndrome

A

Glomerular disease dominated by:

Acute onset of grossly visible hematuria

Mild-moderate proteinuria

HTN

*proteinuria and edema is common, but not as severe as nephrotic syndrome

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27
Q

Rapidly progressive glomerulonephritis (RPGN) definition

A

Signs of nephritic syndrome with rapid decline (days to weeks) in GFR.

Implies severe glomerular injury.

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28
Q

Major pathologic responses of the glomeruli to injury includes…

A

Hypercellularity: native, inflammatory, crescents

Basement membrane: thickening, deposits

Hyalinosis and sclerosis

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29
Q

Physiologic role of visceral epithelial cells

A

Provides a diffusion barrier to filtration of proteins and synthesizes GMB components

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30
Q

Prototypical localizations of immune complexes in the glomerulus: Acute glomerulonephritis

A

Subepithelial humps

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31
Q

Prototypical localizations of immune complexes in the glomerulus: Membranous nephropathy

A

Epimembranous deposits

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32
Q

Prototypical localizations of immune complexes in the glomerulus: Lupus nephritis, Membranoproliferative glomerulonephritis

A

Subendothelial deposits

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33
Q

Prototypical localizations of immune complexes in the glomerulus: IgA nephropathy

A

Mesangial deposits

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34
Q

Antibody-mediated injury to the glomeruli can be from __________ or __________.

A

Fixed intrinsic tissue Ags or Planted Ags

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35
Q

3 example diseases of fixed intrinsic tissue Ags and its associated Ag

A

Anti-GBM nephritis: NC1 domain of type IV collagen Ag

Membranous glomerulopathy: PLA2 receptor Ag

Mesangial Ags

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36
Q

What kinds of Ags can become “planted” in the glomerulus and cause an Ab-mediated injury?

A

Exogenous - DNA and tumor Ags

Exogenous - infectious products

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37
Q

3 immune mechanisms of glomerular injury

A

Ab-mediated injury

Cell-mediated immune injury

Activation of alternative complement pathway

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38
Q

Describe the following patterns of glomerular disorders:

Diffuse
Focal
Segmental
Global

A

Diffuse - all glomeruli involved
Focal - involves only a subset of glomeruli
Segmental - of affected glomeruli, only portions are involved
Global - involves entire glomerulus

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39
Q

The principal glomerular manifestation of progressive injury is…

It eventually leads to…

A

Focal segmental glomerulosclerosis, eventually leading to global glomerular involvement.

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40
Q

Progressive glomerular injury ensues from a…

Progressive glomerular injury is accompanied by…

A

Glomerular and nephron loss, compensatory changes that worsen the injury and eventually cause ESRD.

Accompanied by chronic injuries to other renal structures, usually manifesting as tubulointerstitial fibrosis.

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41
Q

The most common cause of nephritic syndrome is…

A

Immunologically mediated glomerular injury, characterized by proliferative effects and leukocyte infiltration.

42
Q

2 major examples of nephritic syndrome

A

Acute post-infectious glomerulonephritis

Rapidly progressive glomerulonephritis (RPGN)

43
Q

Presentation of the nephritic patient includes…

A 
Hematuria
Red cell casts in urine
Azotemia
Oliguria
Mild-mod. HTN
44
Q

Basic pathological difference of nephritic and nephrotic syndromes

A

Nephritic - inflammation in the glomeruli

Nephrotic - problems with glomerular capillary walls leading to increase permeability to plasma proteins

45
Q

Acute/Diffuse proliferative glomerulonephritis is caused by…

A

Immune complex injury resulting from an exogenous bacterial, fungal or viral infection .

Most commonly it is beta-hemolytic Strep.

46
Q

Acute/Diffuse proliferative glomerulonephritis is characterized by…

A
  1. Marked hypercellularity - ranges from simple mesangial to complex endocapillary infiltrate
  2. Leukocyte infiltration - exudative within glomerular tuft
47
Q

What is seen on electron microscopy in Acute/Diffuse prolferative glomerulonephritis?

A

Subepithelial “hump” of immune complex with neutrophils in the lumen

48
Q

What is seen on immunofluorescence microscopy in Acute/Diffuse prolferative glomerulonephritis?

A

Granular deposits of IgG, IgM and C3 in the mesangium

49
Q

Acute/Diffuse prolferative glomerulonephritis (post-streptococcal) clinical picture in kids:

Age?
When does it occur?
What toxin mediates it?

What is the presentation?

A

Ages 6-10.
Typically from 1-4 wks. following pharyngitis or skin infection.
SpeB (exotoxin B).

Malaise, fever, nausea, oliguria and hematuria for 1-2 wks. after recovery of sore throat.
Dysmorphic red cells, mild proteinuria, periorbital edema and mild/mod. HTN.

^^Nephritic syndrome^^

50
Q

What is the clinical picture of Acute/Diffuse prolferative glomerulonephritis (post-streptococcal) in adults?

A

More atypical and aggressive.
May have sudden HTN or edema, often with elevated BUN.
Nephritic syndrome SX.

51
Q

What is the clinical outcome for kids vs. adults in Acute/Diffuse prolferative glomerulonephritis (post-streptococcal)?

A

Kids: tends to clear in 6-8 wks., renal BX not usually indicated. 95% recover with conservative care.

Adults: only 60% recover completely.

52
Q

RPGN - Crescentic Glomerulonephritis appearance on PAS (4)…

A

Collapsed, compacted glomerular tufts.

Crescent shaped mass of proliferative visceral and parietal epithelial cells.

Obliteration of urinary space.

Infiltration of Mo and leukocytes.

53
Q

RPGN features on electron microscopy (2)…

A

Wrinkling of GBM

Fragmentation of GBM

54
Q

Type I RPGN is…

Disease:

A

Anti-GBM antbody-mediated and renal limited.

Goodpasture syndrome

55
Q

Type II RPGN is…

Diseases (3):

A

Immune complex, idiopathic, post-infectious GN.

Lupus nephritis
Henoch-Schonlein purpura
IgA nephropathy

56
Q

Type III RPGN is…

Diseases (2):

A

Pauci-immune, ANCA-associated.

Granulomatosis w/ polyangiitis
Microscopic polyangiitis

57
Q

Goodpasture syndrome is characterized by…

Effects elsewhere in the body…

High prevalence of patients with…

What unique measure is used as part of a treatment plan?

A

Linear deposits of IgG (sometimes C3) in the GBM, due to a response to non-collagenous regions on collagen type IV.

Cross-reaction w/ lung alveolus causing pulmonary hemorrhage in addition to renal disease.

Patients with certain HLA subtypes and haplotypes (HLA-DRB1) in RPGN patients (genetic predisposition to autoimmunity).

Plasmapheresis to remove circulating Abs.

58
Q

4 diseases treated by plasmaphoresis

A

Goodpasture syndrome
Lupus (cerebritis)
Waldenstrom macroglobinemia
TTP

59
Q

Type II RPGNs are characterized by (2)…

A

Cellular proliferation within glomerular tufts

Crescent formation

60
Q

What is NOT seen in type III RPGN on immunofluorescence or electron microscopy?

A

No anti-GBM Abs or immune complexes on immunofluorescence or electron microscopy.

61
Q

Which syndrome has a greater degree of edema?

Where does it start and progress?

A

Nephrotic syndrome.

Begins periorbitally and progress to generalized edema.

62
Q

Nephrotic range proteinuria is…

A

Protein loss of > 3 gm/day

63
Q

Most common cause of nephrotic syndrome in kids:

A

Minimal-change disease

64
Q

Most common causes (2) of nephrotic syndrome in adults:

A

Focal segmental glomerulosclerosis

Membranous glomerulonephropathy

65
Q

For most (95%) of kids with nephrotic syndrome, it is ascribable to…

A

Primary glomerular disease

66
Q

60% of adults with nephrotic syndrome is due to…

But it is more commonly to be associated with __________ than kids.

A

Primary glomerular disease.

Associated with systemic disease.

67
Q

What is the pathogenesis of nephrotic syndrome?

A

GBM becomes diffusely leaky to protein, especially albumin. It does not usually allow RBCs to transit into the urinary space.

68
Q

Selective vs. non-selective protein loss

A

Selective is loss of albumin only.

Non-selective is loss of any proteins.

69
Q

Primary renal disease vs. secondary renal disease

A

Primary - kidney pathology in absence of an associated systemic disease.

Secondary - systemic diseases causes renal disease (DM, SLE, etc.) with changes in renal histomorphology.

70
Q

3 diseases associated with nephrotic syndrome (rarely exhibit hematuria)…

A

Minimal change disease
Membranous glomerulopathy
Focal segmental glomerulosclerosis

71
Q

2 diseases “classes” associated with nephritic syndrome (more hematuria, less proteinuria)…

A

Acute proliferative glomerulonephritis

RPGN (types I,II,III)

72
Q

2 most common causes of nephrotic syndrome in systemic diseases:

Other causes:

A

DM
SLE

Amyloid, drugs, infections, malignancies, etc.

73
Q

Membranous glomerulonephropathy pathology

A

Approx. 75% due to: AI DZ linked to HLA alleles and Abs to autoAg PLA2 receptor with pathologic involvement of complement (MAC complex) and IgG4.

Remainder is due to drugs, SLE, malignancy, etc.

74
Q

85% of patients with Membranous glomerulonephropathy have…

What info is vital to get before treating?

What kind of proteinuria is seen?

A

Nephrotic syndrome manifestations

If there is a systemic component or if it is primary

Nonselective proteinuria

75
Q

Primary membranous glomerulonephropathy patients respond poorly to…

There is a high reoccurance in…

A

Respond poorly to steroid therapy.

High reoccurence in transplant pts. (40%).

Women may have more benign course.

76
Q

Features seen on PAS in membranous glomerulonephropathy include (3)…

A
  1. Thickening of capillary walls without increase of cellularity.
    • “Spikes” of silver-staining matrix from BM toward urinary space from deposits of IgG.
  3. Effaced foot processes.
77
Q

Clinical course of membranous glomerulopathy

Which treatment is NOT effective generally?

A

Proteinuria persists in 60% of pts., with 40% of them developing renal insufficiency.
10% progress to ESRF.

Corticosteroids are generally not effective.

78
Q

Presenting clinical sign of MCD

What treatment is highly efficacious?

A

Edema in child from 2-6 y/o with nephrotic syndrome SX.

90% of kids with MCD respond well to corticosteroid therapy.

79
Q

MCD has been associated with…

A

Hodgkin lymphoma

80
Q

What kind of proteinuria is seen in MCD?

A

Highly selective proteinuria

81
Q

What is the postulated pathogenesis of MCD?

A

Abs against epithelial cell Ags, toxins, cytokines, etc. cause injury resulting in foot process effacement (fusion). These cells can detach and lead to significant protein leakage thru the GBM.

82
Q

Focal segmental glomerulosclerosis (FSGS) is generally a _____ disease.

It is an adaptive response to…

Inheritance of genes that have what function can cause FSGS?

A

Primary/idiopathic

Adaptive response to loss of renal mass

Genes that encode proteins localized to the podocyte slit diaphragms

83
Q

FSGS accounts for what percent of adults and kids with nephrotic syndrome?

Which races have a higher incidence?

A

Adults - 35% (most common cause of NS in adults in USA)
Kids - 10%

Hispanics and AAs

84
Q

Prognosis of FSGS if it occurs in other diseases is…

20% of pts. with FSGS follow an…

A

A DX with a poor prognosis and will lead to progressive renal disease over time.

20% follow an unusually rapid course w/ massive proteinuria and RF within 2 yrs.

85
Q

How does idiopathic FSGS differ from MCD (and other podocytopathies)? (4)

A
  1. More hematuria, reduced GFR and HTN
  2. Nonselective proteinuria
  3. Poorer response to steroid therapy
  4. Significant progression to CKD with at least 50% developing ESRD within 10 yrs.
86
Q

What kind of syndrome (nephritic/nephrotic) is associated with FSGS?

A

Can be mixed

87
Q

What is HIV-associated nephropathy?

A

FSGS caused by HIV, more commonly in AAs than Caucasians.

88
Q

Membranoproliferative glomerulonephritis (MPGN) ahs what common presentation?

A

Combined proteinuria and hematuria

89
Q

Major histologic findings in MPGN are (3)…

A

Alterations in GBM
Proliferation of glomerular cells, usually in mesangium
Leukocyte infiltration

90
Q

Primary Type I MPGN most commonly presents in…

Common presentation:

50% of pts. develop…

A

Mostly kids and young adults, but can be all ages.

Nephrotic syndrome is common presentation.

CRF over a 10 yr. span.

91
Q

Secondary Type I MPGN most commonly presents in…

Frequently associated with…

It is seen as a reflection of glomerular disease in patients with (3)…

Prognosis:

A

Exclusively adults

Chronic antigenemia causing immune complex deposition

Hep C, chronic immune complex disorders (SLE, endocarditis, etc.). and certain malignancies

Same as primary type I MPGN (CRF over a 10 yr. span)

92
Q

MPGN type II “dense deposit disease” occurs only as…

What is the dominant clinical finding?

Prognosis?

When does occurrence of MGPN II happen frequently?

A

A primary renal disease in kids (no secondary forms in kids or adults)

Hematuria, 50% have nephritic syndrome

Poorer prognosis due to more severe renal disease

Post kidney transplant

93
Q

What is the pathogenesis of MPGN II?

A

C3NeF (nephritic factor) - IgG autoAb that binds C3 convertase causing continuous activation of alternatice complement pathway

94
Q

IgA nephropathy is the most common type of…

A

Glomerulonephritis worldwide

95
Q

Where do IgA deposits occur?

A

Mesangium

96
Q

2 eponymic diseases associated with IgA nephropathy

A

Berger DZ - no systemic DZ

Henoch-Schonlein purpura (HSP) - systemic DZ, with purpura and involvement of the abdominal viscera

97
Q

Who most often gets IgA nephropathy?

What races are at a greater risk?

Family Hx?

A

Mostly a DZ of young adults, mostly in 2nd and 3rd decades, but can occur in older pts.

Caucasians and Asians, less in AAs.

Often a 1st degree relative w/ a Hx of the DZ.

98
Q

What is coincident with the hematuria seen in IgA nephropathy?

A

Coincdient w/ presence of significant infection (URI, GI, abscess, etc.) and recurrence of infection at same site leads to a flare up.

99
Q

2 known associations with IgA nephropathy include…

A

Gluten enteropathy

Liver DZ

100
Q

Clinical outcomes of igA nephropathy

A

Recurrent episodes of hematuria without progression of renal DZ in most pts.

CRF occurs in 15-40% as a slowly progressing DZ over 20 yr. period.

Acute nephritic syndrome w/ HTN in 5-10%

101
Q

Stain for chronic glomerulonephritis

A

Trichrome stain

CPR II Exam #2 (20 decks)

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