Hello everyone, today we are going to study glomerular diseases. The slides are included in this sheet so you

don’t have to go back. GOOD LUCK

There are 4 pathologically important functional units in the kidney: 1) glomerulus 2) tubules 3) interstitium

4) Vessels

In this slide the doctor only add some histological information so I will not mention them you can study them from

the histology lecture

*primary glomerular diseases: the disease mainly affect the glomerulus or may affect many parts but the

glomerulus is the main one

*secondary glomerular diseases: involvement of many organs & one of them is the glomerulus

*the pathogenesis of both primary & secondary glomerular diseases is immune-mediated especially for the

primary and this includes 3 mechanisms:

1) Circulating Ag-Ab complexes that deposit in the glomerulus

2) in situ deposition of Ab: Ab from blood with Ag that is already found in the glomerulus (Ag-Ab complexes are

not found in the blood but the circulating Ab will go to the glomerulus and bind with Ag there).

This Ag can be: a) fixed: which means it’s from one of the components of the glomerulus

b) Planted: which means it deposited in the glomerulus from previous infection & other

mechanisms

3) Anti glomerular basement membrane (Anti-GBM) Ab-mediated glomerulonephritis (GN): Ab bind to specific Ag

in the basement membrane

These notes the doctor add them about the table above:

* renal clinical syndrome: group of signs & symptoms that could be found in laboratory test or whatever that make

a suggestion for a problem in the kidney.

*The most important clinical syndrome that can be from primary glomerular diseases: 1) nephrotic syndrome,

2)nephritic syndrome

*minimal-change diseases, focal segmental glomerulosclerosis, membranous nephropathy,

membranoproliferative GN all of these are nephrotic syndrome

*acute postinfecious GN & IgA nephropathy (both are caused by streptococcal infection) are nephritic syndrome

*from the NET: the difference between nephritic & nephrotic is that in the nephrotic syndrome there is high loss of

proteins in the urine (proteinuria > 3.5 g/day) but in the nephritic syndrome the loss of proteins does not reach the

nephrotic syndrome (proteinuria < 3.5 g/day)

*amyloidosis: caused by many things such as:

1) chronic inflammation ( AA protein)

2) Alzheimer disease (AB protein)

3) multiple myeloma (AL protein)

*amyloidosis can lead to glomerular diseases

*multiple myeloma: malignant plasma cell neoplasm that can produce abnormal immunoglobulin either complete

or light chains we suspect multiple myeloma in a patient with anemia, renal failure & hypercalcemia

*goodpasture syndrome: if the anti-GBM Ab was in the kidney & the alveoli of the lung we call it goodpasture

syndrome

*microscopic polyangiitis secondary to vasculitis

*wegner granulomatosis also secondary to vasculitis

*IgA nephropathy can be alone or with Henoch-scholein purpura

*thrombotic micro angiopathy: two diseases

1)hemolytic uremic syndrome (HUS)

2) thrombotic thrombocytopenic purpura (TTP)

(excessive platelets aggregation in both)

*albort syndrome: deafness & renal failure suspect it

*fabry disease: ............ & renal disorder suspect it

*in general the deposition of Ag-Ab complex will account for complement activation & deposition

Note from doctor

**Sorry for saying that the main manifestation is anemia (I

was talking about Fanconi by mistake)

**But in general it is not uncommon to be complicated by

anemia due to renal insufficiency

**And regarding deafness…I searched and found that

deafness can occur (as part of lysosomal storage disease)

but not as much as Alport (Bilateral sensorineural hearing

loss is often one of the first symptoms of Alport syndrome

and presents in childhood and adolescence)

**and the typical question when you go to clinical is:

deafness+kidney+family history…remember Alport

*no additional notes in this slide

*crescentic glomerulonephritis: sever inflammation of parts of the glomerulus & followed by fibrin deposition & as

a response there will be proliferation of the macrophages & parietal cells & it will deposit at the side of the

glomerulus forming a crescent shape

*remember: membranous nephropathy prefers subepithelial deposition (no mesangium & subendothelial

deposition)

*subepithelial deposition stimulate WBC recruitment in lesser frequency than subendothelial

*IgG attack alpha 3 chain of type 4 collagen

*if it also attack the alveoli of the lung it is called goodpasture syndrome

*in order to diagnose renal disease you need 1)light microscope 2)electron microscope 3)IF

Both of them are capillary because they form the capillary shape (the green color forming circles)