Patologia de glomerulonefrites

The Pathology of

GLOMERULONEPHRITIS

A Tutorial.

byJohn Bradfield

previously Professor of HistopathologyUniversity of Bristol

EnglandUK

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Date created

October 2001

Copyright

Bristol BioMedical

Image ArchiveUniversity of Bristol

UK

Institute of Work

Department ofPathology & Microbiology

University of Bristol

UK

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Glomerulonephritis

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Glomerulonephritis

If that includes you

Help is at hand

Don’t worry

Why is this?……………………………………………….….

Why did I write this tutorial?…………………………………………………...

Because so many beginners find the subject both difficult and confusing.

Usually, because they were taught badly first time round.


After you have worked through this tutorial

You will not only understand:

GLOMERULONEPHRITIS

left click to find out

• the descriptive words used in the classification

•the pathology

•the causes and mechanisms

But you will also be able to:

Help is at hand

• read about glomerulonephritis with interest

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Previous knowledge requirements

Otherwise - left click mouse to proceed to tutorial.

If in doubt

Press this button to try a short test

You need to know a bit about

the normal histology of the human glomerulus.





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Done the test and ready to go?

If you have visited before

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Part 2 = Main tutorial on Pathology of Glomerulonephritis

How to use this tutorial

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Choose

Part 1 = Introduction to the Basic Vocabulary of Glomerulonephritis in general.(A very short section.)

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BASIC VOCABULARY

GLOMERULONEPHRITIS

Welcome to Part 1

Basic Vocabulary

left click to proceed

Let’s start by spending some time on

How to use the words


What is

GLOMERULONEPHRITIS?

Write down your Definition before you proceed

Definition:

Glomerulonephritis is the name given to:

Renal diseases in which

the main abnormality lies in the glomerulus.


Glomerulonephritis

versus

Glomerular diseases


• In spite of the name, “Glomerulonephritis” is often applied to all glomerular diseases, not just those in which there is inflammation (- itis).

• However, when the main feature is deposition of materials in the glomerulus, then these diseases are not traditionally included as glomerulonephritis.

Amyloid Diabetic glomerular disease

Examples ?

Primary

versus

Secondary Glomerulonephritis

• To be honest, which disease falls into which group is more governed by historical precedent than by biological sense.

• What to do?

Secondary glomerulonephritis

is where the glomerular damage is secondary to an

ongoing systemic disease in the rest of the body


Only use the terms in the following way

Examples ? Systemic Lupus Erythematosus Henoch Schonlein Purpura Diabetes Mellitus

GLOMERULONEPHRITIS

Part 1

Basic Vocabulary

This section is now finished.

Click on this button to return to Index Pageto choose next Part





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MAIN TUTORIAL

Part 2 = Main Tutorial

Pathology

of

Glomerulonephritis


Clinical Features

Pathology

Causes and Mechanisms

Eponymous

The KEY to understandingTHE CLASSIFICATION OF GLOMERULONEPHRITISlies in appreciating that :


Each name may call on any of these components

The KEY to understanding GLOMERULONEPHRITIS lies in appreciating that each type is defined using these components.

Clinical Features

Pathology

Causes and Mechanisms

Eponymous

Because of this the next two slides will comprise a short detour into

Clinical ThingsandCauses and Mechanisms


Each name may call on any of these components

One slide onImportant clinical things in glomerular disease

• Age

• Acute versus Chronic

• Clinical patterns

• Proteinuria - Symptomless (revealed only on tests)

- Nephrotic syndrome

• Haematuria - Symptomless (revealed only on tests)

Patient may notice

• Renal failure - (acute or chronic)

• Acute Nephritic Syndrome

• Secondary to other disease


One slide on:Causes and mechanisms in glomerular disease

Primary glomerular disease (Glomerulonephritis)mostly immunological

• Glomerulus is innocent bystander

= Immune complex disease

• Antibodies directed against glomerular components

= Anti-basement membrane disease

• Don’t know

= Immunological mechanisms involved but mechanisms not known

Secondary glomerular disease (Glomerulonephritis and others)variety of mechanisms, some immunological


That ends our various detours and distractions

Now

- at last -

THE PATHOLOGY


There are several things to explore under this heading.You can choose from this list.

Pathology of Glomerular Disease

Use the arrow/hand to click on your choice

1. Patterns of damage

2. Light microscopy = histology

5. Clinical indications for a renal biopsy

6. How a renal biopsy is handled in the laboratory

3. Electron microscopy

4. Immunological

7. Exit tutorial





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PATTERNS OF CHANGE

Welcome to a mini-unit

on

Left click to enter

Biopsy Pathology of Glomerular Disease

Patterns of glomerular damage

Pathological features of glomerulonephritis

Descriptive Terms

Patterns of Damage - 1

All glomeruli normal

= No glomerulonephritis

All glomeruli abnormal

= diffuse glomerulonephritis

Some glomeruli abnormal

= focal glomerulonephritis

(often secondary to

systemic disease)

Left click to proceed

One Glomerulus compared with another


Descriptive Terms


Normal

= No glomerulonephritis

Damage to part

of glomerulus only

= segmental glomerulonephritis

Damage to all parts

of glomerulus only

= globalglomerulonephritis


Within a single glomerulus

There is one further pattern of damage within a single glomerulus thatis important because it:

1. Signifies very bad news

2. Picks out a particular group of patients under the collective title of


Descriptive Terms



Left click to reveal

There is one further pattern of damage within a single glomerulus thatis important because it:

1. Signifies very bad news

2. Picks out a particular group of patients under the collective title of

Otherwise left click in here

Rapidly Progressive Glomerulonephritis is uncommon but very serious.

Click here to learn more about it


Descriptive Terms



Rapidly Progressive Glomerulonephritis





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Causes:

1. Bad end of the spectrum of many mechanismbut especially -

• Anti-basement membrane disease

inluding Goodpasture’s disease

Press here forone slide about

Goodpasture’s disease


Descriptive Terms

Rapidly Progressive Glomerulonephritis

Otherwise left click in here





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Goodpasture’s Disease

Cause:

Specific auto immune immunoglobulin attackon basement membrane’s of1. Capillaries of the glomeruli in the kidneys and2. Capillaries in the lung.

Pathological features:

1. (Cresentic Glomerulonephritis)

2. Deposition of linear IgG and IgM along basement membranes.

Clinical features:

1. Rapidly Progressive Renal Failure

2. Haematuria

3. Haemoptysis


That ends this mini-unit

on


Patterns of glomerular damage

left click in here to return to “Pathology” page





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LIGHT MICROSCOPY


on



Light microscopy

This section describes the

central basis for

the pathological classification of Glomerulonephritis

The way in is to start with

the normal components of the Human Glomerulus

Left click to proceedLeft click to enter

Cells

Endothelial cells

Normally present

Stuff = non-cellular material

Mesangial cellsEpithelial cells

Normally present

Glomerular Basement Membrane

Normal Components of the Human Glomerulus

Click anywhere to seea picture of a normal human glomerulus

against which to compare the various diseases.

A picture of a normal human glomerulusagainst which to compare the various diseases.

Tufts of capillaries

Left click anywhere to proceed

Afferent arteriole

Thinbasement membranes

Bowman’s Space


Nuclei ofglomerular cells

Cells

Endothelial cells

Normally present

Stuff(= non-cellular material)

Mesangial cells

Epithelial cells

Normally present

Capillary Basement Membrane

What can change in disease ?

Too many cells= proliferation

Thickening of thebasement membrane

Mesangium = stalk

First let’s look at changes the previously normal components.

Click to see changes in resident normal cellsNow click to see changes in normal non-cellular stuff.Left click to proceed.

Cells

Endothelial cells

Normally present


Mesangial cells

Epithelial cells

Normally present




Thickening of thebasement membrane

Mesangium = stalk

Now we will look at abnormal components that can appear in disease.

Click when you are ready.

Cells

Endothelial cells

Normally present


Mesangial cells

Epithelial cells

Normally present


Amyloid

Collagen scars (glomerulosclerosis)

Myeloma protein

Diabetic depositsDeposits

Fibrin



Thickening of thebasement membranes

Mesangium = stalk

Only presentwhen abnormal

Only presentwhen abnormal

Left first click to see abnormal cells.Now left click to see abnormal non-cellular stuff.Left click to see how this slide provides the key tothe histological classification of glomerulonephritis.

Inflammatory cells

Too many cells= inflammation.

But still called “proliferation”

HISTOLOGICAL CLASSIFICATION OF GLOMERULAR DISEASE

Some important things

• It is more important to know how the nomenclature and classification worksrather than knowing a great deal about every type of glomerulonephritis.

• The following pictures are for illustration and interest.

You do not need to learn the skill of recognising the diagnosis from the histology.(that important skill is for the renal pathologists alone, and very difficult it often is).

• Many facts are introduced as questions.

If this is your first visit, do not worry if you cannot answer the questions.If you could - you would not need the tutorial.

Click anwhere to proceed

HISTOLOGICAL NAMES USED IN GLOMERULONEPHRITIS

Proliferative glomerulonephritis

Left click anywhere to find out

Too many cells =

What is this called?

Left click anwhere for next


Membranous glomerulonephritis



Too many cells =

Thickening of basement membranes =






Membrano-proliferative glomerulonephritis


Too many cells =


Increase number of cells and thickening of basement membranes =

Have a guess. It’s easier than you think







Minimal Change glomerulonephritis


Too many cells =




Nephrotic syndrome but thickening of basement membranes =







Focal Glomerulosclerosis


Too many cells =



Collagen scars in some glomeruli =




HISTOLOGICAL NAMES USED IN PRIMARY GLOMERULONEPHRITIS






Too many cells =





Click in each box in turn to explore each type in turn

SECONDARY GLOMERULONEPHRITISleft click in here

to return to “Pathology” page.





Please do this now.


Epithelial cells(as “Cresents” inBowman’s space)

Diffuse Proliferative g/n

Proliferative glomerulonephritis (too many cells)

Rapidly Progressive g/n


Inflammatory cells

Endothelial cells

Mesangial cellsMesangio-proliferative g/ntypical of Berger’s disease

Left click anywhere to learn more

Epithelial cells(as “Cresents” inBowman’s space)

Diffuse Proliferative g/n

Proliferative glomerulonephritis (too many cells)

Rapidly Progressive g/n


Inflammatory cells

Endothelial cells

Mesangial cells

Left click anywhereto see a picture

and to read aboutthe clinical correlations

of each

Mesangio-proliferative g/ntypical of Berger’s disease

but

Diffuse proliferative g/n

Too many cells (endothelial and mesangial)Swelling of cells

Normal basement membranes(not visible in this section)

Left click anywhere for clinical correlations

Clinical Correlations

• Presents as acute nephritic syndrome.

• When associated with an acute onset and a recent history of sore throat, this would be characteristic of

post-streptoccocal immune complex glomerulonephritis.

• Can occur in other types of glomerulonephritis,both primary and secondary.

• When post-strep. - excellent prognosis especially in children.Left click a

nywhere for clinical correlations

Left click anywhere for next

but

Mesangio proliferative g/n



Berger’s disease. (hint > Frenchman and so pronounced “Bearjey”.)

Children and adults.

Presents with recurrent painless haematuria=/- proteinuria and hypertension.

Characteristically has IgA deposition in mesangium.

Prognosis good.

Left click a


Left click anywhere for next

Too many mesangial cells

Normal basement membranes

Cresentic g/n (different stain)

Bowman’s space expandedand filled with proliferating epithelial cellsto form a cresent.

Collapsed tufts ofdamaged glomeruli


Left click anywhere for clinical correlationsLeft click a

nywhere for clinical correlationsThat finished this section -left click anywhere to proceed

If 80% of the glomeruli show epithelial cell cresents, this is bad new.

Because of this -The diseases that show this change are usually grouped together under the collective label of Rapidly Progressive Glomerulonephritis (including Goodpasture’s disease).

They present with devastating haematuria and proteinuria and renal failure.

And have a very poor prognosis.







Too many cells =




Neohrotic syndrome but thickening of basement membranes =








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Membranous g/n

Increased thickness ofbasement membranes

No increase in numbers of cells

but



Usually due to chronic immune complex disease. What are the likely antigens? In UK: most - don’t know

but can be malignancy or drugs (penicillamine)

In Japan: Most likely to be Hepatitis B

In some parts of Africa: Most likely to be Malaria

Presents with proteinuria.Commonest cause of nephrotic syndrome in adults in UK.

Left click a

nywhere for clinical correlationsLeft click anywhere to return







Too many cells =












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and

Membrano-proliferative g/n

Too many cells

Thickening of allthe basement membranes



Left click a


There are in fact three types of Membrano-proliferative g/n

Presentation

Proteinuria or Nephrotic syndrome

Left click anywhere for moreLeft click a


If you want to explore theseclick in this box

Otherwise

Left click anywhere else to return







Too many cells =












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Three types of Membrano-proliferative g/n

Left click anywhere to return

Type 1 = Mesangiocapillary g/n

• Immune complex mediated

• Causes mostly unknownSome associated with infections, drugs, tumours, etc.

• Many associated with persistent C3 hypocomplementaemia

• Course = progressive deterioration

Type 2 = Dense deposit disease

• Related to activation of the alternate complement pathway

• Dense deposits in basement membrane are not immune complexes

Type 3

• Rare







Too many cells =












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Minimal change glomerulonephritis

Light microscopy (histology)


Electron microscopy

- essentially normal

- fusion of epithelial cell foot processes. (this is not specific for any one type of glomerulonephritis. It correlates with heavy proteinuria.)

Left click a

nywhere for clinical correlationsLeft click anywhere to return


Cause unknown

Presents with steroid responsive nephrotic syndrome.

Commonest (90%) cause of nephrotic syndrome in children aged 1-5 in UK. These children are not usually biopsied.

Rapid response to steroids.

Prognosis

Children - excellent. Adults - variable.







Too many cells =












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Focal glomerular sclerosis



Presents with proteinuria.

In UK. Cause of 10%-15% of nephrotic syndrome.

Also associated with other diseases (secondary g/n)

Left click a


Collagen scar tissue (stained red)in some glomeruli but not othersand in one part of the glomerulus

Prognosis

Most patients eventually develop end stage renal failure.








Too many cells =












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Autoimmune diseaseswith immune complexes as the

mechanism of glomerular damage

It is convenient to group these under three headings

SECONDARY GLOMERULONEPHRITIS

Metabolic diseasesvarious mechanisms of glomerular damage

Vascular diseasesvarious mechanisms of glomerular damage

Otherwise left click anywhere else to return

for more on eachleft click in here







Too many cells =












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Autoimmune diseaseswith immune complexes as the mechanism of glomerular damage


left click anywhere for next

Examples include

Systemic lupus erythematosusvariety of pathological patternsvariety of clinical presentations

Henoch-Schonlein purpura

clinical patterns include nephrotic syndromeand rapidly progressive g/n


Examples include

Diabetes mellitusWhole range of patterns of damage to kidneysWhole range of patterns of damage in glomeruli.Cinically glomerular damage causes proteinuria

nephrotic syndrome and renal failure.

Renal amyloidIn virtually all patients with systemic amyloid.Presents as proteinuria/nephrotic syndrome -

often presenting feature. Inevitable renal failure

Metabolic diseasesvarious mechanisms of glomerular damage


Diabetic nodular glomerulopathy

There is a variety of different ways in which diabetes mellitus affects the glomeruli

This is the pattern that is usually illustrated in books -not because it is the commonest, but because it is the most specific for DM.

and because it has a long eponymous name = Kimmelsteil-Wilson lesion.(you only need to remember it if you hare going for the gold medal.

It’s more important to know thisfact:half of patients with childhood onset DM die in renal failure



Examples include

Microscopic Polyarteritis nodosaDifferent disease than classical PAN.Prognosis untreated very poor but

very good response to immuno-suppression.

Haemolytic-uraemic syndromeClinically - acute nephropathy, haemolysis and thrombocytopaenia.

Prognosis depends on type:Childhood (better prognosis)Adult (poorer prognosis)Secondary (poorer prognosis)

Vascular diseasesvarious mechanisms of glomerular damage

left click anywhere to return







Too many cells =












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That ends the mini-unit

on

Biopsy Pathology of Glomerular Disease

Light microscopy






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ELECTRON MICROSCOPY


on


Electron microscopy

Left click anywhere to enter

ELECTRON MICROSCOPY

Click anywhere to proceed

Electron microscopy makes some important contributions

• to the understanding of the glomerulus in health

• to the understanding of mechanisms of disease

• in diagnosis

Changes with Proteinuria

Normal Appearances

Immune Complex Disease

Click within a box to find out more about each in turn

Otherwise click in here to return to

Pathology page

ELECTRON MICROSCOPY

• Here I have selected for you the three topics that I think are most relevant.

• Of these the first section is by far the most important.





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Here is our standard histological light microscope picture of a normal human glomerulus

Now let’s imagine that we could peer

at great magnificationinto Bowman’s space

andlook at the external

(downstream) side of one of these capillaries.

Left click anywhere to proceedLeft click anywhere to proceed

NORMAL APPEARANCES

The next slide will be a scanning electron microscope pictureof exactly this - at great magnification




And here we are


Bowman’s space

We are now in Bowman’s space

andhere are all the capillaries.

Left click anywhere to proceedLeft click anywhere to proceed

Bowman’s space


Now let’s wind up the magnification even furtherand look at the outside (downstream) side of one single calillary

And this is what we would see


Bowman’s space

The downstream side of allthe capillaries are clothed in

epithelial cells thathave complicated

interdigitating patternsthat are traditionally called

foot processes.


Now let’s break open this capillary and look insideto see the upstream side of the filter

which is the endothelial lining of the blood capillary.

Bowman’s space

Left click anywhere to do this and see inside the capillary

Left click anywhere to see labelsLeft click anywhere to proceed

Bowman’s space

And here is the endothelial celllining of the blood capillary.

Look at the 3.5nm poresin the endothelial cell lining.

These hold back the blood cellbut allow plasma access

to the basement membranefilter underneath.

Here again is the downstreamside of the filter

with the interlacing footprocesses of theepithelial cells.


Now let’s see what this would look like ina conventional electron transmission microscope

which is a very thin section in two dimensions only


Now let’s see what this would look like ina conventional electron transmission microscope

which is a very thin section in two dimensions only

And here is theendothelial cell liningof the blood capillary.

We can hardly see

the poresin the endothelial cell lining.

Here are the foot processes of the epithelial cells.

Left click anywhere to see labels

Red cells


Red cells


In diagnostic pathology transmission electron microscopyis usually used, rather than scanning electron microscopy


Normal Appearances




Pathology page

ELECTRON MICROSCOPY







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Proteinuria is associated with a change in the configuration of the interlacing pattern of the epithelial cell foot processes.

On scanning electron microscopy the processes become simplified so that the outer surface of the basement membranes is covered in sheets rather than processes.

This configuration can be seen on the more usual transmission electron microscopy., where it is historically known as “fusion of the foot processes”

Comments:1. Correlates with heavy proteinuria.2. ? cause ? effect ?3. Not specific to any particular type of glomerulonephritis.

CHANGES WITH PROTEINURIA

Page one of one


Normal Appearances




Pathology page

ELECTRON MICROSCOPY







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Although immune complexes can be identified by immunofluoresence, it is sometimes helpful to know exactly where these deposits are in relation to the basement membranes.

IMMUNE COMPLEX DISEASE

Click anywhere to see examples

(Page one of three)

Immune complex disease

Sub-epithelial deposits in post-streptococcal g/n

Click anywhere to see another example

(Page two of three)

Immune complex disease

Click anywhere to return

(Page three of three)

Deposits within thickened basement membranes in membranous g/n


Normal Appearances




Pathology page

ELECTRON MICROSCOPY







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on


Electron microscopy






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IMMUNOLOGY


on


Immunological investigation of a

renal biopsy.


IMMUNOLOGY

• Antibodies are prepared, specific for abnormal things that might be present in the diseased glomerulus.

• A fluorescent molecule is attached to the back end of the antibody molecule so that the molecule will be visible down the light microscope under ultra-violet light.

• Thin sections are cut from the frozen fresh material.

• These are then “stained” using specific antibodies prepared in the laboratory.

• The “stained” sections are viewed under ultra-violet light.

• Positive “staining” appears as green fluorescence on a black background


IMMUNOLOGY

Antibody molecule

Antigen-specific terminal

Fluorescent molecule

Target material

Tissue section

Glass slide


IMMUNOLOGY

Usually three variables are scored.

1. Identity of abnormal materials in glomerulus.

Usually patient’s own immune reactants egIgGIgMIgAC3

2. Where is it? eg In capillary loopsIn mesangium

3. What is it like? eg lumpy-bumpy granularlinear

Left click anywhere to see three examples

Which immune reactants?

IgG +/- IgMComplement C3

Left click anywhere for next example

Interpretation ?

Immune complex deposition

Pattern ?Lumpy-bumpy granular

Where?

in walls of glomerular capillaries

Left click anywhere last example

Interpretation ?

Anti-basement membrane disease (Goodpasture’s)

Pattern?

Linear


IgG +/- IgMComplement C3

Where?

in walls of glomerular capillaries


Interpretation ?

Berger’s IgA disease

Pattern ?Granular


IgAComplement C3

Where?

In mesangial stalks

There are several things to explore under this heading.You can choose from this list.


Use the arrow/hand to click on your choice

1. Patterns of damage

2. Light microscopy = histology

5. Clinical indications for a renal biopsy

6. How a renal biopsy is handled in the laboratory

3. Electron microscopy

4. Immunological

7. Exit tutorial





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on


Immunological investigation of arenal biopsy






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CLINICAL INDICATIONS FOR A RENAL BIOPSY


on


Clinical indications for a renal biopsy


(three slides only)


General principles

• Making a diagnosis

• Planning treatment

• Deciding when not to treat

• Assessing prognosis



• Proteinuria with impairment of renal function

• Symptomless isolated proteinuria if more than 2g/day

• Nephrotic syndrome in adultsIn children it is most likely to be due to steroid sensitiveminimal change g/n so trial of steroids is less risky than biopsy.

• Persistent haematuria with proteinuria especially if there is renal impairment.

• Acute renal failure if likely to be renal on origin, as opposed to pre-renal (hypovolaemic shock) or post-renal (obstructive) in origin.

• Chronic renal failure with normal sized kidneys

• Renal transplant dysfunction

• Systemic disorders with features that include haematuria, proteinuria and renal failure.


• Asymmetric kidneys

• Tiny shrunken kidneys

• Obstructive renal disease

• Coagulation defects

• Acute infections


SOMECONTRA-INDICATIONS FOR A RENAL BIOPSY


on



Clinical indications for a renal biopsy





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BIOPSY


on


How a renal biopsy is handled in the laboratory


One slide only

HOW A RENAL BIOPSY IS HANDLED IN THE LABORATORY

For histology(light microscopy)

For electronmicroscopy

Forimmuno-fluorescence

Core of fresh tissue

Dissected into three partsensuring some glomeruli in each


That ends the one page mini-unit

on



How a renal biopsy is handled in the laboratory

They don’t come any more “mini” than that.





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left click mouse to proceed.

Try this short test to find out whether you need to revise some basic things about the human glomerulus.

Revision Test: The structures of the nephron.

Can you name these eight components of the nephron?

Write down the 8 answers before you proceed.

Then left click to see all the answers.

1.

2.

5.

3.

8.

7.

4.

6.

Glomerulus Tubules


Don’t cheat.

There’s no point.

You are only cheating yourself.


1.

2.

5.

3.

8.

7.

4.

6.

Glomerulus Tubules


Have you written downall 8?

Don’t proceed untilyou have.

The next slide givesthe answers.

Then left click to see all the answers.

1.

2.

5.

3.

8.

7.

4.

6.

Glomerulus Tubules

1. Afferent arteriole

3. Efferent arteriole

4. Capsule of glomerular sac

2. Glomerular capillaries

5. Proximal convoluted tubule

6. Loop of Henle

7. Distalconvolutedtubule

8. CollectingDuct


left click to continue the short test

left click for all of the answers.

Revision Test : Components of the Glomerulus

Can you list?

The five important components of the normal human glomerulus.

Cells

1. ???

lining the capillaries.2. ???downstream of thebasement membranes.

3. ???

controlling cellsin the supporting stalk.

Non-cellular components

4. ???

this is the actual filter.

5. ???

the supporting stalk.

left click for next.

The five important components of the normal human glomerulus

Cells

1. Endothelial cells -

lining the capillaries.

2. Epithelial cells - downstream of the basement membranes.

3. Mesangial cells -

in the mesangial stalk.

Non-cellular components

4. Capillary Basement Membranes - this is the actual filter.

5. Mesangium -

the supporting stalk.

Revision Test : Components of the Glomerulus

1.

2.

3.

4.

left click for all of the answers.

Revision Test: Clinical Manifestations of disease

Can you list the clinical manifestations of

glomerular disease = Glomerulonephritis?

1. Haematuria.

2. Proteinuria.

3. Renal failure.

4. Any combination of these.

left click for next

The clinical manifestations of

glomerular disease = Glomerulonephritis?

Revision Test: Clinical Manifestations of disease

How did you get on?

If you struggled with the quiz - I suggest that you Work through a tutorial on Bristol Biomed entitled “Understanding the Glomerulus”. It will take you about 15 minutes, and has some excellent animations.

When you get back you will then be equipped to conquer the subject of

GLOMERULONEPHRITIS.


To return to the main tutorial on Pathology of Glomerulonephritisleft click on this button

To exit and return to Bristol Biomed for a background tutorial on the Glomerulusleft click on this button

http://www.brisbio.ac.uk/bblt/res.html





Please do this now.


I hope that this tutorial has been useful.

If you liked it,

or didn’t,

or have any suggestions:

Then please let me know on: [email protected]

Left click anywhere to find the exit

How to EXIT THE TUTORIAL

To return to first page of this tutorial -left click within this button

To shut down if you are in Outlook Express or Netscape -right click the mouse and select “End Show”then close the browser in the usual way.

To return to Bristol BioMed -left click within this button

To shut down if you are in Powerpoint -right click the mouse and select “End Show”then close Powerpoint in the usual way.

There is no need to “save” this program

http://www.brisbio.ac.uk/bblt/res.html

Patologia de glomerulonefrites

Education

Transcript of Patologia de glomerulonefrites