Week 9 Flashcards
How are glomerular dx classified
- Clinical Presentation
- Histomorphology
- Primary vs. Secondary
Primary vs. Secondary
○ Primary –> Limited to the kidney (renal abnormalities are the presenting symptom)
○ Secondary –> typically some sort of systemic disease and abnormalities going on elsewhere and it just so happens to involve the kidney
How does strep infection cause injury to your kidney?
- etiologies: complex, misinterpretation, antigen
• Bacterial antigens and antibodies deposit into the kidney
- Antigens form immune complexes and deposit which induces an inflammatory response in the kidney which damages the kidney tissue
- Molecular mimicry: form an antibody against one of the antigens on the bacteria that also can bind to intrinsic components of the glomerular filtration barrier
- Antigen can deposit/implant/lodge in the wall of the glomerulus which causes secondary (in-situ) binding to form an immune complex. This leads to inflammation which can be complement mediated or recruitment of innate immune system cells. (This is the most common etiology. )
What would you do for work up/evaluation for patient showing signs of streptococcal glomerulonephritis
- C3 complement count, CH50 –> complement would be decreased as all of the complement gets used up
- Antistreptolysin O level –> this is an antibody against one of the streptococcal antigens
- Urinalysis: You can have red urine from things other than blood in the urine ; Check for protein ( to rule out nephrotic syndromes)
- Microscopic analysis: Allows you to look for casts
What is a RBC cast?
- significance?
- RBC gets lodged in the tubules and take on the shape of the tubules –> eventually get passed into the urine but they retain their shape
- Shows you that there is some sort of problem early on in the nephron. It could be glomerular injury or something proximal in the tubule. RBCs need time to accumulate and form a cast
What is a dysmorphic RBC?
- indicates?
- RBCs are abnormally shaped because of mechanical injury. There is some sort of damage to the glomerular filtration barrier and they are having to squeeze through
- When you see dysmorphic RBC described or see a picture of them, that indicates that there is some glomerular injury going on
Histo findings in Acute Proliferative Glomerulonephritis
○ Hypocellularity-the black dots are the nuclei of all the cells (this is where the name proliferative comes from)
○ Larger glomerulus overall because there are a lot more cells
○ Proliferation of mesangial ( kind of fibroblasts/myofibroblasts of the kidney) and endothelial cells and infiltration of inflammatory cells because it is an inflammatory process
Difference in progression of disease in child vs elderly w/ glomerulonephritis
- treatment in adults vs child
- elderly will have progression more quickly in his disease/more quickly develop this clinical picture
○ In a child, the glomerulus will heal fairly quickly. You use supportive measures, fluids, antibiotics
○ Adults, especially older or immunocompromised adults have a poorer outcome after initial injury and have two possible outcomes: If it becomes extremely aggressive, you could have acute kidney failure (RPGN: rapidly progressive glomerulonephritis). Occurs when patient (usually adult) doesn’t respond to treatment or doesn’t get treatment soon enough OR if acute proliferative glomerulonephritis takes a little while to resolve and they end up with scarring which causes glomerular sclerosis
RPGN: Crescentic Glomerulonephritis
- why is it called crescent? what is it made up of? where are they located?
- how do cells get there?
○ Crescent (moon-shaped) made up of fibrin, monocytes, macrophages in the outside of the Bowman’s space (parietal epithelial cells)
- Damage to glomerulus after strep leading to necrosis of endothelial cells & mesangial cells & podocytes, and eventually will break down the filtration barrier almost completely in areas, which will allow for cells to leak through so monocytes & macrophages that have already been recruited will leak out into that space & they will also damage the parietal epithelial cells, which will then start producing collagen & laying down fibrinous matrix (most significant damage –> wipes out foci of the glomerulus filtration barriers allowing cells to enter the Bowman’s space) and over time more & more fibrin gets deposited, which can compress the glomerulus (can see in the R picture that the glomerulus is small again) & causes more severe symptoms
categories of RPGN?
1) pauci-immune disease (mediated by ANCAs but no immune complexes identifiable by FISH, still have damage to filtration barrier) 2) Goodpasture syndrome or anti-GBM (anti-glomerular basement membrane antibodies)
What pattern of injury will the patient eventually end up with after it progresses to irreversible injury (glomerular necrosis)?
He will end up with scarring after wound healing. In the kidney we call it sclerosis, instead of fibrosis.
How would you describe the typical reaction pattern that we get in kidneys? (3 types)
Focal (only involves some glomeruli, not all of them) & segmental (only involves part of the glomeruli, not all of it) so this pattern is called focal segmental glomerulosclerosis & the other option would be diffuse global glomerulosclerosis (diffuse = involves all the glomeruli & global = involves the entire glomerulus). Focal segmental glomerulosclerosis is a pattern of injury that can be primary or the end stage of almost any kind of kidney disease.
What renal dx causes edema?
- nephrotic syndomre bc loss of proteins in urine causes decrease in oncotic pressure
What is required for the dx of nephrotic syndrome?
- albunminuria > 3.5 g/day
- hypoalbuminemia <3g/dL
- peripheral edema
Dx for 4 yr old with edema, 4+ protein in urine, BUN and creatining normal, and normal renal biopsy on light microscopy?
- pathogen
- Minimal Change Disease (Nephrotic Syndrome)
- Epithelial injury that causes early findings like podocyte defacement (flattened out), allowing for small proteins (albumin) to escape through (mechanism is unclear, we don’t know)
