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Flashcards in nephrosis 1 Deck (16):

what is the most common cause of nephrotic syndrome in children? What changes do you see?

MCD. No change by light microscopy. electron micro. shows podocyte changes (effacement and fusion and sometimes villous transformation)


What causes the changes seen in MCD?

disruption of SGPs leads to loss of neg. charge and then fusion of fp and aggregation of actin filaments


Diabetic nephropathy: pathogenesis

non enzymatic glycation of proteins, decreased proteoglycans, increased TGF-beta and ROS. Thickened GBM and TBM traps proteins and GFR declines


describe affect of DM on GFR

at first it increases (superhyperfiltration) due to poor HS-PG depostion->^pore size and decrease charge(->proteinuria). Then it declines due to protein trapping.


describe the proteinuria in DM

Initially (microalbuminuria) the selectivity for albumin is high then as you get more proteinuria its less selective


what meds do we prescribe in pts with early signs of diabetic nephropathy? Why?

ACEI. it reduces superhyperfiltration which damages glomerulus


Describe amyloid

inert fibrilar protein. criss-cross pattern. 8-10 nm thick. Birefringent due to beta-pleated sheets


what happens in amyloidosis?

proteins precipitate and deposite in mesangium w/o hypercellularity


Focal segmental glomerulo-sclerosis: what type of proteinuria? History of? what glomeruli? What happens? what gets deposited? Special cells/

nonselective. H/O MCD, Heroin, HIV, Ureter reflux. Juxtamedullary. SEGMENTAL deposits of IgM and C1q in hyaline segments. Foam cells (lipid in mesangial cells)


How does a low protein diet help in diabetic nephropathy?

you decrease the hyperfiltration and the proteinuria


Idiopathic membranous nephropathy (IMN): H/O? What deposits and where?

neoplasms, hepatitis, tx w/ gold or penicillamine. IgG and C3 immune-complex deposits in SUBEPITHELIUM, NOT mesangial matrix (as in lupus)


what are two subsets of IMN?

Antigen-excess dz, Heymann nephritis (autoab's against megalin and antiphospholipase A2 receptor)


SLE: first signs? other signs?

butterfly rash; proteinuria, hematuria, casts


Two principle presentations of SLE?

Diffuse (nephritic) and membranous (nephrotic). Diffuse has worse prognosis due to lots of abnormal serology (more ANAs, circulating immune complexes, cryo Igs, etc)


hwo can lupus nephritis progress?

nephrotic->nephritic but not other way around.


membranous lupus GN: characteristic glomerular changes. Where do complexes deposit

thick GBM w/ immune deposits. Karyorrhexis (fragmenting nuclei in areas of hypercellularity). subepithelial and mesangial deposits.