Glomerulonephritis and histology of the glomerulus Flashcards
1
Q
What is glomerulonephritis?
A
- Inflammation of glomeruli
- Often involves immune system
2
Q
What 4 structures of the glomerulus can be damaged in glomerulonephritis?
A
- Capillary endothelium
- Glomerular basement membrane
- Mesangial cells
- Podocytes
3
Q
What is nephrotic syndrome?
A
- Podocyte damage
- Leading to glomerular charge barrier disruption
- Massive proteinuria
- Causes oedema (to the point that the face swells like in an allergic reaction)
4
Q
How does proteinuria lead to oedema?
A
- Loss of albumin
- Oncotic pressure of blood is reduced
- Hydrostatic pressure remains the same
- Reduction in osmotic pressure in capillaries
- Can’t move fluid out of interstitium back into circulation
- Fluid pools in extremities
5
Q
Which triad of signs/symptoms is associated with nephrotic syndrome?
A
- Proteinuria >350 mg/mmol
- Hypoalbuminaemia
- Oedema
- (usually accompanied by high cholesterol)
6
Q
What are other features of nephrotic syndrome?
A
- BP often normal (though can be low or high)
- Creatinine may be normal
7
Q
What are the primary causes of nephrotic syndrome?
A
- Minimal change disease
- Membranous glomerulonephritis
- Focal segmental glomerulosclerosis (FSGS)
8
Q
What are the secondary causes of nephrotic syndrome?
A
- Diabetes
9
Q
How does diabetes damage the kidneys?
A
- Excess glucose binds to proteins
- Especially at efferent arteriole
- Hyaline atherosclerosis obstructs blood flow
- Initially GFR increases
- Over time mesangial cells secrete more structural matrix
- Basement membrane thickens
- GFR decreases
10
Q
How is diabetic nephropathy treated so that it does not lead to renal damage?
A
- Treat hypertension
- Good glycaemic control
- ACE inhibitors
- Angiotensin receptor blockers
11
Q
What is minimal change disease?
A
- Most common cause of nephrotic syndrome in children under 6
- No significant renal changes are seen under light microscope
- Prognosis good in children, variable in adults
- Glomerular capillaries fuse with foot processes of podocytes
- Filtration barrier not formed
- Patients loose lots of proteins
- Swollen in eyes and face due to oedema
12
Q
What is membranous glomerulonephritis?
A
- Subepithelial deposition of immune complexes
- Thickening of basement membrane
- 40% adult nephrotic syndrome
13
Q
How is membranous glomerulonephritis treated?
A
- Immunosuppressants
- Treatment of underlying cause
14
Q
What is FSGS?
A
- Occurs in some glomeruli but not all
- Only affects some segments of affected glomeruli
- Podocytes damaged
- Proteins build up in glomerulus (hyalinosis) leading to sclerosis
15
Q
What are the causes of FSGS?
A
- Primary: idiopathic
- Secondary: sickle cell disease, HIV, heroin abuse, kidney hyperperfusion
16
Q
How is FSGS treated?
A
- Treatment with steroids
- Inconsistent results can lead to chronic renal failure
17
Q
How is nephrotic syndrome managed?
A
- Oedema is treated with diuretics (may need IV) and salt and fluid restriction
- ACE-Inhibitors - anti-proteinuric
- Treat underlying condition
18
Q
What is the triad of nephritic syndrome?
A
- Haematuria
- Reduction in GFR (renal impairment/oliguria)
- Hypertension (due to activation of RAAS caused by decreased GFR)
19
Q
What are the other features of nephritic syndrome?
A
- Often some proteinuria but less than nephrotic syndrome
- Disruption of endothelium results in inflammatory response and damage to glomerulus
- Onset may be acute or rapidly progressive
20
Q
What are some common causes of nephritic syndrome?
A
- IgA nephropathy (Berger’s disease)
- Rapidly progressive glomerulonephritis
- Goodpasture’s (Anti GMB)
- Post-streptococcal GN
21
Q
Outline IgA nephropathy
A
- Most common primary glomerular disease worldwide, causing recurrent haematuria
- Hypertension and IgA levels raised
- Deposited in mesangium
- Sclerosis of damaged segment
- 20% will develop advanced CKD
22
Q
How is IgA nephropathy treated?
A
- Control BP with antihypertensives
- Steroids
23
Q
What is rapidly progressive glomerulonephritis?
A
- Severe glomerular injury
- Leakage of fibrin
- Macrophages and epithelial cells proliferate
- Crescent shaped masses form and reduce glomerular blood supply
- Loss of renal function within days to weeks
24
Q
How is rapidly progressive glomerulonephritis treated?
A
- High dose steroids
- Immunosuppressants
- Plasma exchange
25
What is Goodpasture's Syndrome?
- Antibodies to type IV collagen in glomerular basement membrane develop
- Inflammation
- Results in rapidly progressive glomerulonephritis, acute renal failure, lung haemorrhage
26
How is Goodpasture's Syndrome treated?
- Plasma exchange (remove antibodies)
- Corticosteroids (remove inflammation)
- Prognosis poor without treatment
27
What is post-streptococcal glomerulonephritis?
- Presents 1-3 weeks following group A beta-haemolytic streptococcal infection of tonsils, pharynx or skin
28
How is post-streptococcal glomerulonephritis treated?
- Antibiotics to treat remaining infection
- Prognosis excellent in children
- ~60% adults recover completely (rest develop hypertension or renal impairment)
29
How is nephritic syndrome managed?
- ACE-I or AIIR and salt restriction control BP and reduce proteinuria
- Treat oedema with diuretics and salt and fluid restriction
- Disease specific treatment (immunosuppressants)
- Stop smoking, statins etc to manage cardiovascular risk
- Dialysis (often short-term)
