glomerular disease Flashcards
what happens to the glomerulus in nephrotic syndrome
basement membrane becomes very permeable to protein and protein leaks into the urine
presentation of nephrotic syndrome
proteinuria
hypoalbuminemia
oedema
can also have hypertension, hypercoagulability, hyperlipidaemia
general management of nephrotic syndrome
high dose steroids
low salt diet
diuretics
albumin infusions if needed
what is the most common cause of nephrotic syndrome
minimal change disease
how does minimal change disease present
usually presents after an illness like gastroenteritis
oedema ascites
small pleural effusions
investigations in minimal change disease
bloods for low albumin <12mg/mmol
urine dipstick -
what will a urine dipstick in minimal change disease show
protein 3+
blood 2+
management of minimal change disease
prednisolone for 8 weeks
what should you use if the minimal change disease relapses >4x a year
immunosuppressants
- cyclosporin
- tacrolimus
- rituximab
if the minimal change disease is not responding to steroids what other diagnosis should you consider
focal segmental glomerulosclerosis
is focal segmental glomerulosclerosis nephritic or nephrotic
nephrotic
what age group is most likely to be effected by focal segmental glomerulosclerosis
young adults
what can cause FSG
HIV
alport’s syndrome
sickle cell anaemia
investigations for FSG
renal biopsy
management of FSG
ACEi/BP control
supportive
may need transplant
what is Alport syndrome
congenital X linked defect in type IV collagen
what group does alports syndrome normally affect
young males
pathophysiology of alports syndrome
defect in type IV collagen causes a defective GBM
presentation of alport’s syndrome
microscopic haematuria
progressive renal failure
bilateral sensineural deafness
management of alports
transplant
what is nephritic syndrome
inflammation in nephrons
presentation of nephritic syndrome
haematuria
less proteinuria than in nephrotic syndrome
reduced kidney function
pathogen in post infectious glomerulosclerosis
usually group A strep
pathophysiology of post infectious glomerulosclerosis
strep antigens deposit in glomerulus and antibodies form complexes
initiates immune response in kidney resulting in tissue injury
nephritis
investigations in post infectious glomerulonephritis
throat swab for tonsillitis
blood test for antibodies
management of post-infectious glomerulonephritis
it is self limiting so most of the time it just needs supportive management
antibiotics if needed
diuretics and anti-hypertensives to stop overload
pathophysiology of IgA nephropathy
immune complex formation in circulation
complexes deposit in the kidneys and cause inflammation and injury
presentation of IgA nephropathy
nephritic syndrome
1-2 days after UTI
older children
biopsy results in IgA nephropathy
IgA deposits and glomerular mesangial proliferation
urine dipstick findings in IgA nephropathy
macroscopic haematuria
proteinuria
management of IgA nephropathy
ACEi in mild disease
supportive treatment
immunosuppression - cyclophosphamide
steroids
what is henoch-schonlein purpura
a variant of IgA nephropathy
pathophysiology in HSP
small vessel vasculitis with IgA deposits
presentation of HSP
5-15 year olds 1-3 days after a trigger like URTI purpuric rash with 1 of: - abdominal pain - arthritis or arthralgia - renal involvement - biopsy showing HSP
biopsy findings in HSP
IgA deposits
glomerular mesangial proliferation
management of HSP
treat symptoms
glucocorticoids for GI involvement
immunosuppression with cyclophosphamide
what should be screened for long term in HSP
hypertension
proteinuria
