Glomerular Pathology Flashcards
what characterises nephrotic disease
- proteinuria
- oedema
- high cholesterol
why is oedema seen in nephrotic disease
the increase protein in the urine reduces the oncotic pressure in the blood
where does the damage in the nephron occur in nephrotic disease
podocytes primarily but also the basement membrane
what are 3 primary causes of nephrotic disease
- minimal change glomerulonephritis
- FSGS
- membranous glomerulonephritis
what is minimal change glomerulonephritis
where circulating factors damage the podocytes meaning they don’t selectively filter as well
what age ranges minimal change glomerulonephritis seen
children
what is FSGS
where circulating factors damage podocytes and cause glomerulosclerosis
what is glomerulosclerosis
where fibrosis occurs in the glomerulus
what age range is FSGS seen
adults
what can be used to manage minimal change glomerulonephritis
steroids - as these suppress the immune system
what is membranous glomerulonephritis
where immune complexes deposit into the podocytes
what immunoglobulins are involved in the immune complexes seen in membranous glomerulonephritis
IgG
give 2 secondary causes of nephrotic disease
diabetes and amyloidosis
true or false: steroids help in the management of FSGS
false
what is nephritic disease
where there is blood lost in the urine
what characteristics are seen in nephritic disease
haematuria and hypertension
where in the nephron is damaged in nephritic disease
blood vessels
gives some causes nephritic disease
- alport syndrome
- goodpastures syndrome
- Thin GBM
- vasculitis
what is alport syndrome
where there is abnormal type 4 collagen meaning blood can pass through the walls of the of the GBM easier
what is the first change that occurs in diabetic nephropathy
hyperfiltration and increased GFR
what is goodpasture syndrome
where there is an anti-GBM antibody which leads to inflammation of the glomerulus and holes punched in the GBM allowing the passage of blood
what is IgA nephropathy
where IgA is deposited in the mesangia causing an immune response and inflammation of the glomerulus - this means blood can filter through
what is IgA vasculitis
where there is an anti neutrophilic cytoplasmic antibody activation which causes neutrophils to break down the GBM
what systemic effect is seen in IgA vasculitis
purpura
why are proteins filtered during hyper filtration in diabetic nephropathy
the increased glucose is mostly reabsorbed by the SLGT 2 transporters with salt - this means less salt reaches the macula dense resulting in dilation of the afferent and constriction of the efferent arteriole - this means more blood is in the glomerulus increasing the pressure
what happens to the basement membrane in diabetic nephropathy
it becomes thicker due to an increase in glomerular pressure
what happens to the podocytes in diabetic nephropathy
they become injured
what happens to the afferent and efferent arterioles in the later stages of diabetic nephropathy
they both undergo fibrosis, making the lumen smaller - this decreases the GFR
what are kimmelstiel-wilson nodules
fibrotic nodules that appear in the glomerulus due to too much glucose
what is the microalbuminuria stage of diabetic nephropathy
where the GFR decreases back to normal
the GBM thickens, the podocytes are damaged and the mesangia expands
first time you can detect protein in the urine
what is overt proteinuria
where the GFR falls rapidly giving systemic hypertension (due to less salt delivery to the macula densa)
what is given to manage diabetic nephropathy
ACE inhibitors
statins
change in diet and exercise
how do ACE inhibitors help in diabetic nephropathy
they prevent the actions of angiotensin 2 which causes an increase in permeability to proteins, mesangia expansion and construction of the efferent arteriole
what is hypertensive nephrosclerosis
where high blood pressure causes chronic kidney disease
what other signs will a patient with hypertensive nephrosclerosis have
LV hypertrophy, hypertensive eye disease
true or false: hypertensive nephrosclerosis develops rapidly
false - it has a slow progression
how is renal artery stenosis different to hypertensive nephrosclerosis
renal artery stenosis causes the hypertension whereas the chronic kidney disease is caused by the already present hypertension in hypertensive nephrosclerosis
what happens to the GFR in renal artery sclerosis
it falls rapidly
how do acute falls in blood pressure damage the kidneys
damage of the endothelium causes microangiopathic haemolytic anaemia
fibrosis of the efferent arteriole leads to necrosis and RAAS activation
which arteriole undergoes fibrosis in hypertensive nephropathy
efferent arteriole
