20 - Glomerular Disease 2 Flashcards Preview

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Flashcards in 20 - Glomerular Disease 2 Deck (35):
1

minimal change disease etiology/pathogenesis

etiology unknown
thought to involve T cell derived circulating permeability factor that directly damages podocytes and permeability barrier

2

who gets minimal change disease?

children (most common nephrotic syndrome in children)
adults in 5th-6th decade

males > females

3

presentation of minimal change disease

nephrotic syndrome
sudden onset proteinuria and edema
otherwise nl renal function
HTN and hematuria UNcommon

4

minimal change disease lab findings

hypoalbuminemia, nl complement

5

minimal change disease biopsy findings

LM - nl glomeruli
EM - podocyte foot process effacement/fusion
IF - negative

6

focal segmental glomerulosclerosis etiology/pathogenesis

primary idiopathic cases due to circulating factor (SuPAR) that directly injures podocytes

7

who gets focal segmental glomerulosclerosis?

young adults
also can be seen in kids w/ minimal change disease that relapses

more common in african americans

people w/ HIV, obesity, heroin use

8

presentation of focal segmental glomerulosclerosis

nephrotic syndrome
may have HTN, renal failure or microhematuria

9

focal segmental glomerulosclerosis lab findings

hypoalbuminemia
nl complement levels

10

focal segmental glomerulosclerosis biopsy findings

LM - focal sclerosis (duh), only part of glomerulus affected (segmental)
EM - podocyte foot process effacement/fusion
IF - negative

11

membranous nephropathy etiology/pathogenesis

autoimmune - ab directed against phospholipase A2 receptor on podocytes
immune complex deposition and complement activation

12

who gets membranous nephropathy?

MCC idiopathic nephrotic syndrome in adults (5th-6th decades peak)
males > females
most idiopathic, but some assoc w/ cancer (lung, breast, GI), hep B, SLE

13

clinical presentation of membranous nephropathy

nephrotic syndrome
HTN and renal failure UNcommon

14

membranous nephropathy lab findings

hypoalbuminemia
nl complement
check for assoc conditions (hep, ANA, cancer)

15

membranous nephropathy biopsy findings

LM - thickening of glomerular BM
EM - subepithelial immune deposits
IF - granular deposits of Ig and complement along BM

16

membranoproliferative GN etiology/pathogenesis

immune mediated glomerular injury
trapping circulating immune complexes > complement activation
circulating "nephritic factor" spontaneously activates complement on capillary wall

17

who gets membranoproliferative GN?

any age
female > male
often assoc w/ hep C**, other infections, SLE, cryoglobulinemia

18

presentation of membranoproliferative GN

nephrotic syndrome
many also have nephritic syndrome
HTN (often early)

19

membranoproliferative GN lab findings

low complement
if assoc w/ HCV - cryoglobulins, rheumatoid factor

20

membranoproliferative GN biopsy findings

LM - thickening of glomerular BM, glomerular cell prolif (usually mesangial)
EM - subendothelial immune deposits
IF - subendothelial pattern of C3 and IgG

21

postinfectious GN etiology/pathogenesis

usually after group A strep infxn
circulating immune complexes from response to infxn lodge in glomeruli > activate complement

22

how long does it take to get postinfectious GN?

14-21 d after infxn (sooner for throat than skin)

23

presentation of postinfectious GN

nephritic syndrome
edema, sudden weight gain in children
HTN - often severe
renal failure common

24

postinfectious GN lab findings

pos ASO titer, pos streptozyme
low complement levels

25

postinfectious GN biopsy findings

LM - diffuse prolif and inflam
EM - subepitheial "humps"
IF - lumpy-bumpy IgG and C3 deposits

26

IgA nephropathy etiology/pathogenesis

immune mediated - IgA containing complexes
deposit in mesangium

27

who gets IgA nephropathy?

MCC primary glomeulonephritis
young adults
asians and caucasians > blacks
male > female
may have simultaneous pharyngitic or GI viral infxn

28

presentation of IgA nephropathy

asymptomatic hematuria, nonnephrotic proteinuria, nl or mildly reduced renal fn
rarely, will be much more severe

29

IgA nephropathy lab findings

inc serum IgA in 50%
nl complement

30

IgA nephropathy biopsy findings

LM - mesangial cell prolif and matrix expansion
EM - mesangial deposits
IF - globular mesagial IgA deposits

31

Anti-GBM nephritis etiology/pathogenesis

ab against type 4 collagen in glomerular BM
may be accompanied by pulm hemorrhage (Goodpasture's syndrome)

32

who gets Anti-GBM nephritis?

young adults
male > female
assoc w/ autoimmune disorders (goodpasture, ANCA assoc vasculitis)

33

presentation of Anti-GBM nephritis

rapidly progressive glomerulonephritis w/ crescent formation

34

Anti-GBM nephritis lab findings

pos anti-GBM ab
nl complements

35

Anti-GBM nephritis biopsy findings

LM - crescent formation
EM - breaks in glomerular BM, no deposits
IF - linear IgG deposits along BM