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Renal - Gupta > Intro to Renal Pathology > Flashcards

Intro to Renal Pathology Flashcards

1
Q

What 4 Categories do all renal diseases fall into?

• what is the typical pathological cause?

A

4 general areas effected:

• Glomeruli - typically IMMUNE mediated

• Tubules - Tend to be from TOXIC or INFECTIOUS agents (e.g. exsanguination causes low BP leading to tubule necrosis)

• Interstitium - tend to be from TOXIC or INFECTIOUS processes

• Blood Vessels

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2
Q

What type of imaging is required following a medical biopsy?

• what is the purpose of getting this biopsy?

A

1. light microscopy

2. Immunofluorescence

3. Electron Microscopy

Purpose: Diagnosis, Prognosis, and Guide Therapy

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3
Q

****What component has been stained black by this silver stain?

A

basement membrane mostly composed of type IV collagen that stains black with silver stain

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4
Q

***what components are represented by each color?

  • where would subendothelial deposits be found?
  • what about subendothelial deposits?
A
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5
Q

****What is represented by the following arrows?
• short single arrow?
• long single arrow?
• double arrow?

• relationship between the two single arrows?

A
  • Short Single: Tubular Basement Membrane
  • Long Single: Glomerular Capillary Basement Membrane
  • Double arrow: Mesangial Cells and Mesangial Matrix
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6
Q

What is the purpose of the mesangial cells?

A

Mesangial Cells and Matrix provide structural support to the glomerulus

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7
Q

****Electron Micrograph

A
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8
Q

****Electron Micrograph

A
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9
Q

****Electron Micrograph

A
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10
Q

****Electron Micrograph

A
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11
Q

What are Nephrin and Podocin?

• what would be the problem with having a mutation in one of these genes?

A

Nephrin and Podocin = slit pore diaphragm proteins

**Without these proteins there is deficient filtration and massive proteinurea

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12
Q

Describe the pathology of this glomerulus.

A

focal segmental glomerulosclerosis (FSGS)

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13
Q

What are the NPHS1 and NPHS2 genes?

• what happens when you lose functionaligy of these genes?

A

NPHS1 - NEPHRIN - results in Focal Segmental Glomerulosclerosis

NPHS2 - PODOCIN - results in Focal Segemental Glomerulosclerosis

Clinically - these people will have huge amounts of protein in their urine

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14
Q

What are some Primary Glomerular Diseases?

A

• Minimal-change disease

• Focal segmental glomerulosclerosis

• Membranous Nephropathy

• Acute postinfectious GN

• Membranoproliferitive GN

• IgA nephropathy

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15
Q

What are some Hereditary causes Glomerular Disease?

A
  • Alport Syndrome
  • Fabry Disease
  • Podocyte/slit-diaphragm protein mutations (e.g. podocin, nephrin)
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16
Q

What are some secondary causes of Glomerular Disease?

A
  • Lupus Nephritis (SLE)
  • Diabetic Nehpropathy
  • Amyloidosis
  • GN secondary to Multiple Myeloma
  • Goodpasture Sydrome
  • Microscopic Polyangiitis
  • Wegner Granulomatosis
  • Henoch-Schonlein Purpura
  • Bacterial Endocarditis
  • Thrombotic microangiopathy
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17
Q

What is the most common cause of Glomerular Injury?

A

circulating immune complexes are formed in the glomerulus or are circulating and deposit in the glomeruli.

deposition leads to leukocyte recruitment and complement systems are activated

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18
Q

*****Describe what has happened in this kidney biopsy?

  • most likely process mediating this disease?
  • what do you need to do to confirm a Dx?
A

RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS

• Leukocytic Infiltration (exudation) INTO the glomeruli

  • Variable proliferation of Mesangial and Partietal Epthithelial Cells
  • Disease is most likely mediated by Immune Complexes in the ENDOTHELIUM or SUBENDOTHELIUM

• Need EM or Immuno Stains to determine location of deposition

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19
Q

How can you attempt to differentiate between Endothelial/Subendothelial and Subepithelial Immune Deposition on H and E?

• reason for this?

A

Endothelial/Subendothelial
• Typically presents with Inflammatory Reaction and Exuberent Proliferation of Glomerular Cells - inflammation is a result of being so proximal to capillaries of the glomerulus (w/ WBCs etc. inside)

Subepithelial
• non-inflammatory region because further from glomerular capillaries

20
Q

What makes an antibody “in situ”?

A

Its directed against actual components of the Glomerulus

21
Q

When do you see granular and linear patterns of Immune Deposition?

A

Granular:
• Deposition of CIRCULATING immune complex

• Deposition of antibodies against GLOMERULAR antigen (membranous nephropathy)

Linear:
• ANTI - GBM antibody deposition (e.g. Goodpastures syndrome)

22
Q

****What pattern of immunofluorescence is shown here?
• Antibody type?

A

Linear immunoflurescence is shown with anti-GBM antibody

Shown below is a granular pattern of deposition

23
Q

****What is pauci immune deposition what does it look like?

A

Immunstaining with no real pattern and very little fluorescence - essentially looks like normal tissue

Picture of this is shown below

24
Q

Post-Streptococcal Glomerulonephritis

  • disease type
  • cause?
  • Inflammatory or noninflammatory?
  • Appearance
A

• Immune Complex Disease - caused by antibodies against streptococcal pyogenic exotoxin B

• complexes deposite in the subepithelial layerso typically noninflammatory

• results in the appearance of subepithelial (epithelial cell) HUMPS

25
Q

****Shown here are subepithelial humps above the basement membrane.
• what disease/process has caused this appearance?
• What will immunofluorescence look like?

A

Post-streptococcal Glomerulonephritis caused by immune complex deposition in subepithelial layer

• because this antibody is located in SUBepithemilium we expect GRANULAR IMMUNO-FLUORESCENCE

26
Q

****What protein is being targeted by the antibodies shown here?
• Symptoms of a person with this disease?

A

This is a typical linear deposition pattern seen in a glomerulus of GOODPASTURE’S Syndrome

ANTI-GBM antibodies specifically for TYPE IV collagen

Symptoms:

• Shortness of Breath

• Coughing up Blood (Remember Type IV also VERY important in LUNGS)

• Fever

• Unplanned Weight Loss

• Fatigue

27
Q

What are the characteristics of Rapidly Progressive Glomerulonephritis?

• consequences of not treating it?

A
  • Progressive Loss of Renal Function
  • lab findings typical of nephritic syndrome
  • often SEVERE oliguria

***Failure to treat can lead to death from Renal Failure in weeks to months***

28
Q

****What are some characteristic histological findings of Rapidly Progressive Glomerulonephritis?

A

Crecents in Bowman Space = KEY (aka Crescentric Glomerulonephritis)

29
Q

****What causes the pathology seen here?

A

Rapidly Progressive Glomerulonphritis (crescentric GN) can be caused by a number of diseases

•~1/2 have immune complex GN with cresents and ~1/2 have pauci-immune crescentric GN

30
Q

What findings are typical of Pauci-immune type crescentric GN?

A
  • Can’t Detect Immune complex deposition via Electron Microscopy or Immunofluorescence
  • Antineutrophil Antibodies (ANCAs p or c) typically found in the serum
  • Glomeruli show Segmental Necrosis and Breaks in the Basement Membrane of the Glomerulus
31
Q

****What is going on here?

• key features?

A
  • Sclerosis can be seen in the Top Left (possibly old vessel or glomeruli)
  • Inflammatory Cells are surrounding the Glomerulus
  • Glomerulus is Fibrotic at the Center with Cells infiltrating Bowman Capsule
32
Q

What 3 diseases involve the vessels of the Glomerulus?

A

• Arterionephrosclerosis

• Malignant HTN

• Thrombotic Microangiopathies

33
Q

T or F: Hydrostatic pressure in glomerular capillaries is lower than in other tissues.

A

FALSE, Pressure is HIGHER (50 mmHg) in glomerular capillaries vs. 35mmHg in others. Also, its significantly higher than the pressure in Bowman Space

34
Q

What 3 things tend to happen if you put more pressure than normal in Glomerular Capillaries?

A
  • GBM thickening
  • **mesangial cell hypertrophy
  • Hyperplasia and mesangial matrix production**
35
Q

****What is shown here?

• what would this kidney look like grossly?

A

Pink Protein Deposits in the Vessel on the right side of the image from Hyaline Arteriosclerosis

Additionally you can see extensive interstitium present indicating that there is scaring

Grossly you can see the Lumpy Bumpy Appearance

36
Q

What does chronic High Blood Pressure do to Glomeruli?
• what is the term used for END STAGE hypertensive nephropathy?

A

• Hyaline Sclerosis of afferent arterioles causes gradual narrowing of the LUMEN leading to ISCHEMIC ATROPHY (glomeruli get smaller)

• ARTREIONEPHROSCLEROSIS

37
Q

***What is seen here?

• Key Features?

A

Arterionephrosclerosis
Sclerosis and Shinking down of Glomeruli (ghost glomeruli) Leads to Hypertrophy of Remaining Glomeruli

38
Q

What is the result of malignant HTN on the Glomerulus?

A

Causes Fibrinoid Necrosis - due to increased permeability of small vessels to fibrinogen and other plasma proteins, endothelial injury, and platelet Deposition

**usually you’ll be told the pt. had really high BP so you can differentiate between this and fibrinoid necrosis.

39
Q

****What is shown here?

A

Fibrinoid Necrosis from Malignant HTN

40
Q

T or F: hyperplastic arteriosclerosis and arterial fibrinoid necrosis are specific for malignant HTN.

A
41
Q

False

A
42
Q

****How do you expect the gross appearance of a kidney with Malignant HTN to differ from that of a pt. with benign HTN?

• what are some characteristics of this syndrome as a whole?

A

petechial hemorrhages from rupture of capillaries give rise to FLEA BITTEN APPEARANCE

• you can also see edema from huge amt. of fluid getting pushed into kidney

• Syndrome Characteristics: Papilledema, Encephalopathy, Cardiovascular Abnormalities, and Renal Failure

43
Q

****What has happened to this patient?

A

Thrombotic Microangiopathy - you can see deposition of fibrin and thrombin in the glomerular capillaries

44
Q

***What are some Primary Causes of Thrombotic Microcangiopathies?

A

Primary:
•HUS (usually in kids who get E. coli O157 with shiga toxin)
• aHUS (mixture of inherited an aquired, unknown etiology)
• ADAMST13 deficieny

Seconday:
• DIC

• Malignancy

45
Q

*****What is the likely explanation for the appearance of the two most lateral kidneys that both came from the same individual?

A

Chronic Kidney Disease has caused these kidneys to become symmetrically atrophied and scared

46
Q

****What has likely caused this appearance?
• Key Features?

A

Chronic Kidney Disease

KEY PTS.
* Advanced Scarring (possibly to the point of sclerosis)
* Thyroidization of Tubules (see top right)
* arteriolar hypertrophy

Renal - Gupta (17 decks)

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