Nephrotic syndrome Flashcards
Nephrotic syndrome characteristics ?
Hypoalbumaenia > 3,5 g/day
Proteinuria > 3,5 g/day
Hyperlipidaemia –> consequence low albumin
oedema –> salt & water retention
Management nephrotic syndrome
dietary Na retention and thiazide diuretic + normal protein intake
anticoagulants due to hypercoagulable state due to loss clotting factors
statins for lipid abnormalities
ACE-i for reducing proteinuria
Minimal change nephropathy (MCN)
fusion foot processes podocytes
no antibodies / immunecomplexes
mostly in children, boys, oedema face
MCN treatment
symptomatic + high-dose corticosteroids
Congenital nephrotic syndrome
loss of function of nephrin, normally in filtration slit
effacement foot processes + abnormale glomeruli
progresses to ESKD
Primary focal segmental glomerulosclerosis (FSGS) patho + symptoms
massive proteinuria, haematuria, hypertension, renal impairment
IgM deposits & complement in glomerulus
Focal tubular atrophy, interstitial fibrosis, effacement podocytes in normal & sclerosed glomeruli
5 histological variants primary FSGS
classic –> sclerosis anywhere glomerulus
Glomerular tip lesion –> sclerosis at tubular pole
Collapsing –> enlarged podocytes, HIV associated
Perihilar –> sclerosis around hilum + hyalinosis
Cellular –> proliferation occluding capillary lumen
Secondary FSGS
number of functioning nephrons reduces –> still working nephrons hypertrophy, hyperfiltration, hydraulic injury
hypoalbuminaemia unusualy, heavy proteinuria
Membranous glomerulopathy + treatment
Autoimmune, men, asymptomatic proteinuria
uniform thickening capillary basement membrane
Treat –> spontaneous remission or ACE-i
Amyloidosis + treatment
Disorder of protein folding –> insoluble fibrils deposited extracelullarly
eosinophilic deposits + kidneys enlarged
Treat –> renoprotective + reduce production amyloidogenic protein
Diabetic nephropathy
DM type 2 –> vasoactive factors cause hyperfiltration + enlargement kidney
GBM thickens, mesangium expands, depletion podocytes
Treat by treating DM
