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GI and Renal Exam 1 > 15 - Glomerular Disease Pathology II > Flashcards

15 - Glomerular Disease Pathology II Flashcards

1
Q

What is the first approach to diagnosing your patient with renal disease?

A

Classify the patients clinical symptoms using clinical and laboratory parameters into one of the clinical renal syndromes

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2
Q

Describe nephritic syndrome

A

EMPHASIZED

  • HTN*** (due to salt retention)
  • Oliguria (due to decreased GFR from inflamed glomeruli)
  • Proteinuria (more than 150 mg/24 hrs BUT less than 3.5 g/24 hrs)
  • Hematuria*** (with dysmorphic RBCs)
  • RBC casts***

Know the starred things

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3
Q

Describe nephrotic syndrome

A

EMPHASIZED

  • Proteinuria*** (with more than 3.5 g/24 hrs **)
  • Generalized pitting edema* and ascites (due to hypoalbuminemia*)
  • Hypercoagulable state
  • Hypercholesterol
  • Hypogammaglobinemia
  • Fatty casts ***

Know the starred things

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4
Q

Describe the cause of nephritic syndrome

A
  • Due to breaks in the glomerular capillary loops

- Erythrocytes spill out into urinary space

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5
Q

Describe the cause of nephrotic syndrome

A
  • Due to glomerular capillary filtration defects

- Protein molecules spill out into the urinary space

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6
Q

What is effacement?

A
  • Shortening and/or thinning of the epithelial cell foot processes
  • This causes protein defects (nephrotic syndrome)
  • This process can no longer stay attached to the basement membrane, so they will detach and the basement membrane will be leaky
  • Protein can be reabsorbed

???

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7
Q

What is the cause of acute renal failure?

A
  • Due to tubular injury in most cases
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8
Q

Describe the progression of renal disease

A
  • Acute renal failure, nephrotic syndrome and nephritic syndrome can all occur
  • If not treated or if it does not respond to treatment, all can progress to CHRONIC RENAL FAILURE (scarred or fibrosed kidneys)
  • There will be a slow rise in creatinine over months to years
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9
Q

What are the gross features of CRF?

A
  • Kidneys are small
  • Cortex thinned
  • Increase pelvic fat
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10
Q

What are the microscopic features of CRF?

A
  • Glomerular sclerosis
  • Interstitial fibrosis
  • Tubular atrophy

KNOW SLIDE 39 (image of these pathologies)

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11
Q

What are the causes of nephrotic syndrome?

A

Primary causes

  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy

Secondary causes
- Diabetic nephropathy

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12
Q

What are other systemic disorders that can cause nephrotic syndrome?

A
  • Diabetes
  • Amyloidosis
  • SLE
  • Drugs (gold, penicillamine, heroin)
  • Infections (malaria, syphilis, Hep B, Hep C, HIV)
  • Malignancies (carcinoma, melanoma)
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13
Q

Describe minimal change glomerulopathy

A

AKA minimal change disease or lipoid nephrosis

  • **MOST COMMON CAUSE OF NEPHROTIC SYNDROME IN CHILDREN **
  • Age 2-6 years old
  • Normal glomeruli on LM and IF imaging ***
  • Effacement of foot processes will be visible on EM ***
  • Lipid tubular cells
  • Usually responds to steroids
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14
Q

What do you NEED to remember about minimal disease?

A
  • NOTHING will be seen on LM or IF

- EFFACEMENT of FOOT PROCESSES on EM

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15
Q

What is the KEY LESION in minimal change disease?

A
  • Diffuse epithelial foot process effacement ****
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16
Q

What will you see in the tubular cells in minimal change disease?

A
  • Lipids in tubular cells
  • AKA “lipoid nephrosis”
  • Tubular cells contain lipid, hence the name “lipoid nephrosis”
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17
Q

Describe focal segmental glomerulosclerosis (FSGS)

A

Proteinuria is a defining feature of FSGS

Incidence = 7 /million; increasing over recent years

Cardinal feature is progressive glomerular scarring

Early in the disease course, glomerulosclerosis is focal and segmental. With progression, more diffuse and global glomerulosclerosis develops.

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18
Q

What are the causes of focal segmental glomerulosclerosis (FSGS)?

A

EMPHASIZED***

  • Heroin
  • HIV

Primary
- Idiopathic disease (80%)

Secondary

  • Virus-induced: HIV, CMV, EBV, Parvovirus B19
  • Drug-induced: Heroin, anabolic steroies
  • Family/genetic: mutations in podocyte genes
  • Adaptive (hemodynamic adaptations): systemic hypertension, surgical renal ablation, aging kidney, sickle cell anemia, BMI (obesity; bodybuilding)
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19
Q

Describe the disease characteristics of focal segmental glomerulosclerosis (FSGS)?

A
  • Nephrotic syndrome (or nephrotic-range proteinuria)
  • Hypertension (common)
  • Common in African Americans
  • Variable degree of decreased renal function
  • Microscopic hematuria
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20
Q

Describe the biopsy resutls of focal segmental glomerulosclerosis (FSGS)

A
  • LM: Segmental sclerosis *** (this means only a SEGMENT of the glomerular capillary tuft is involved - “hyalinosis”
  • IF: Mild IgM and C3 or negative
  • EM: diffuse epithelial cell injury (foot process effacement)
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21
Q

Describe the clinical course of focal segmental glomerulosclerosis (FSGS)

A
  • Response to steroids is variable

- Thus, differs from minimal change disease in prognosis

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22
Q

What are the causes of membranous glomerulopahty?

A
  • Idiopathic (85%)
  • 60% will develop “waxing and waning” proteinuria
  • 15% go on to “classic nephrotic syndrome
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23
Q

What was EMPHASIZED about membranous glomerulopathy?

A

Deposition of Ag-Ab complexes

24
Q

What will you see on renal biopsy of membranous glomerulopathy?

* KNOW THIS*

A
  • LM: thickened capillary walls; “spikes” on silver stain
  • IF: granular IgG and C3 along the GBM
  • EM: subEPITHELIAL deposits

** KNOW subepithelial and NOT subendothelial ***

25
Q

What type of antibody can be detected via IF in membranous glomerulopathy?

A

IgG *****

No other type

26
Q

Describe Membranoproliferative glomerulonephritis (MPGN)?

A

DO NOT CONFUSE WITH MEMBRANOUS GLOMERULOPATHY

Usually nephrotic syndrome with a nephritic component (hematuria)

27
Q

Describe the disease process of MPGN

A
  • slowly progressive course
  • steroids and immunosuppressive agents NOT effective
  • 50% progress to chronic renal failure within 10 yrs
28
Q

Describe the etiology of MPGN

A

Can be idiopathic or 2º to chronic immune diseases

29
Q

What is the basic pathology of MPGN

A

Mesangial hypercellularity

PLUS

Capillary wall remodeling (with the formation of double contours)

30
Q

What do we see in type 1 and type 2 MPGN?

A

Type 1 MPGN
- SubENDOthelial deposits

Type 2 MPGN
- Intramembranous deposits

**Predominant mesangial involvement ** KNOW THIS

31
Q

Describe the pathology of MPGN

A
  • thickening of the GBM (membrano) and proliferative mesangial cells
  • reduplication (“splitting”) of the GBM (“tram tracks”)
32
Q

What are the two types of MPGN?

A
  • Type I (subendothelial deposits)

- Type II (intramembranous deposits)

33
Q

Describe MPGN type 1

A

Cause: Primary (idiopathic) or secondary to chronic immune complex disorders (SLE, Hep B, Hep C, cryoglobulinemia, endocarditis, CLL/lymphoma)

Not important

34
Q

Describe the biopsy findings of MPGN type 1

A

Pathology

  • LM: “tram tracks” (on silver stain) ** KNOW TRAIN TRACKS*
  • IF: granular C3 (and often with IgG)
  • EM: subendothelial and mesangial deposits (mesangial interpositioning between endothelial cells and GBM)

This is SUBENDOTHELIAL, NOT subepithelial ***

35
Q

Describe MPGN type 2

A
  • 70% have C3 nephritic factor (C3NeF; an autoantibody which stabilizes C3 convertase, protecting it from enzymatic degradation)
  • therefore, persistent C3 activation and consumption, causing hypocomplementemia
  • *****low serum C3 !!!
36
Q

Describe the pathology seen in renal biopsy of MPGN type 2

A

Pathology

  • LM: “tram track” (on silver stain)
  • IF: C3 only
  • EM: Intramembrane deposit, lamina densa - electron dense material (“dense deposit”)
37
Q

What are the features of nephritic syndrome?

A
  • Patient complains of dark colored urine
  • Microscopic analysis of the urine will show erythrocytes in urine
  • The patient may also have renal failure (increase in serum creatinine and blood urea nitrogen/BUN_ in which case this is called ACUTE nephritic syndrome
38
Q

What are the two conditions that cause acute nephritic syndromes?

A
  • Diffuse proliferative glomerulonephritis
  • Crescentic glomerulonephritis

Both of the above are NOT diseases per se, but descriptive pathological changes. There are each associated with specific diseases.

39
Q

What are the causes of diffuse proliferative GN?

A

Acute post-strep GN

40
Q

What are the causes of crescentic GN?

A

1 - Goodpasture’s disease
2 - Lupus nephritis
3 - ANCA-associated diseases

41
Q

Describe acute glomerulonephritis

A

Hematuria, azotemia, oliguria, in children after a latent period of 1-3 weeks following a strep infection

Old term: POST-STREPTOCOCCAL
New term: POST-INFECTIOUS

Can be from Staph, Pneumococcus, Meningococcus, viruses (Hep B & C, mumps, HIV, varicella, EBV), and parasites (malaria, toxo)

95% full recovery

42
Q

Describe acute post-streptococcal GN

A
  • Affects children
  • History of respiratory infection 2 weeks prior
  • Only certain “nephitogenic” strains of beta hemolytic streptococci cause this
  • Acute nephritic syndrome
  • Renal failure (usually moderate)
  • Hypertension
  • **LOW complement 3 levels (C3) **
  • ASO titer serially elevated

Just remember that the C3 levels in the serum are low because they are all accumulating in the kidney

43
Q

Describe the pathological findings on renal biopsy of post-strep GN

A
  • LM: diffuse proliferative GN with neutrophils (KNOW NEUTROPHILS ***)

IF: scattered granular (“starry sky”) IgG, IgM, and C3 along GBM and in the mesangium

EM: subepithelial “humps” IgG, IgM, C3 along GBM FOCALLY (KNOW subEPIthelial ***)

44
Q

Descrie diffuse proliferative glomerulonephritis

A
  • Endocapillary proliferation

- Note glomerulus suffused with inflammatory cells occluding capillary loops

45
Q

Describe acute post-strep GN on pathology slides

A
  • Enlarged, hypercelluar glomeruli with endothelial and mesangial cell proliferation
  • IgG and C3 irregularly distributed along the basement membrane (“starry sky”) and in the mesangium***
46
Q

What do you need to remember about post-infectious glomerulonephritis?

A

Post-infectious glomerulonephritis: subepithelial “humps” as well as mesangial and subendothelial deposits.

47
Q

What is crescentic glomerulonephritis?

A
  • Crescentic glomerulonephritis is a form of glomerular disease in which glomerular crescents are formed
  • Crescents cause severe glomerular injury
  • Severe renal failure and death can result if untreated
48
Q

What will you see on slides of crescentic glomerulonephritis?

A
  • Cellular crescentic proliferation of cells lining the Bowman’s space
  • Compressed capillary loops
49
Q

What fills the “cresentic” shape?

A
  • Anti-GBM Ab
  • ICs
  • Anti-PMN Ab
50
Q

What are the components of the crescents in crescentic GN?

A
  • Plasma constituents into Bowman’s space, including coagulation factors and inflammatory mediators
  • Fibrin forms and there is then proliferation of epithelial cells from the parietal wall of Bowman’s capsule, as well as influx of monocytes/ macrophages, resulting in crescent formation.
51
Q

What will you see in type 1 (Goodpasture disease)?

A
  • Linear “cigarette smoke” appearance

- Capillary loops outlined by linear anti-basement membrane antibodies

52
Q

What will you see in type 2 (lupus)?

A
  • Lumpy bumpy granular appearance

- Capillary loops are outlined by granular immune complex deposits

53
Q

Describe anti-GBM disease (Goodpasture disease)

A

It is an anti-glomerular basement membrane antibody disease

  • It is an autoimmune disease characterized by abnormal production of antibodies directed against Collagen IV (which constitutes the basement membrane of the glomerulus, lung, etc.)
  • This results in vasculitis, especially in the lung and kidney, causing the pulmonary-renal syndrome
  • Causes crescentif GN in the kidney
  • Serum anti-GBM antibody level will be elevated
  • Needs to be treated with high dose of steroids, cytotoxic agents and PLASMAPHERESIS***
54
Q

What causes crescentic glomerulonephritis due to immune complex disease?

A
  • Lupus nephritis

- IgA nephropathy/Henoch-Schonlein purpura

55
Q

Describe pauci-immune crescentic GN (ANCA associated GN)

A
  • A group of vasculitic disorders especially affecting small vessels (i.e. small arteries, capillaries, arterioles, veins, etc.)
  • Can cause the pulmonary-renal syndrome
  • Often associated with Anti-Neutrophil Cytoplasmic Antibody (ANCA)
  • Immune deposits in glomeruli are either absent or minimal
  • A classic example is Wegener’s granulomatosis
56
Q

What was EMPHASIZED about rapidly progressive glomerulonephritis (RPGN)?

A
  • It is a CLINICAL definition, NOT a specific pathologic one

- It is MOST associated with crescentic GN ***

57
Q

What do you NEED to review and focus on for the exam questions?

A

Review

  • Cartoons of histology
  • Focus on LM, IF, and EM *****
  • Pay attention to the process of the podocytes
  • Know where the immune complex or antibody is (subepithelial or subendothelial *****)

GI and Renal Exam 1 (16 decks)

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