Glomerulonephritis Flashcards
damage to what cells can lead to vasculitis
mesangium
endothelial cells
damage to podocyte leads to what
non-proliferative lesions and protein in urine
damage to endothelium leads to what
proliferative lesions and red cells in urine
presentation of GN
haematuria AKI/CKD HTN Nephtotic or nephritic syndrome proteinuria
presentation of nephrotic syndrome
proteinuria >3g hypoalbuminaemia fluid retention and oedema hypercholesterolaemia renal vein thrombosis pulmonary emboli volume depletion vitamin D deficiency subclinical hypothyroidism
presentation of nephritic syndrome
AKI oliguria oedema/fluid retention HTN active urinary sediment
classification of proteinuria
microalbuminuria
asymptomatic proteinuria
heacy proteinuria -3g
nephrotic syndrome >3g
non-immunosuppressive management GN
antihypertensives <130/80 ACEI/ARB diuretics statins anticoag/aspirin/antiplatelet fish oil
immunosuppressive management GN
pred azathioprine cyclophosphamide cyclosporin mycophenolate plasmapharesis IV Ig Monoclonal Ab
general management of nephrotic syndrome
fluid and salt restriction ACEI/ARB antiagulate IV albumin if volume depletion diuresis
what is complete remission from nephrotic syndrome regarded as
<300mg protein/day
what is partial remission from nephrotic syndrome regarded as
<3g/day protein
what is minimal change GN, who is it more common in, how is it managed
injury to podocyte and effacement of foot process
children
respond to steroids
what is FSGS and what causes it
focal segmental glomerulosclerosis
HIV, heroin, obesity, reflux nephropathy
how is FSGS managed
steroids, some have chronic disease
what is membranous GN, what causes it, how does it appear on biopsy
injury to podocyte
heb B, lupus, gold, penicillamine
management of membraneous glomerulonephritis
steroids, alkylating agents, b cell monoclonal Ab
what Ab is present in membranous GN
anti-PLA2r-Ab
most common GN
IgA nephropathy
presentation of IgA nephropathy
asympatomatic haematuria
macroscopic haematuria after infection due to rising IgA
can cause HSP
how many with IgA nephropathy progress to ESRF
25% in 10-30y
describe the pathophysiology of membranoproliferative GN
thickening of capillary wall and proliferation of mesangial cells
immune complex deposition and complement activation due to infection or myeloma
what is RPGN
rapidly progessive GN
rapid deterioration of renal function over days/weeks
active urine sediment
common causes of RPGN
GPA, MPA
goodpastures
IgA HSP
what antibody is found in Goodpastures
anti-GBM
management of RPGN
pred
cyclophosphamide/mycophenolate/azathioprine
plasmapharesis
describe the formation of an immune crescent
neutrophils bind to Ab leading to capillary being torn open and inflammatory cells entering bowmans capsule
glomerulus becomes crushed and dies
