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Path 4 > Renal: glomerular disease > Flashcards

Renal: glomerular disease Flashcards

1
Q

nephritic syndrome

A

hematuria, proteinuria, azotemia, oliguria, edema, HTN

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2
Q

azotemia

A

increased BUN and Cr d/t dec GFR

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3
Q

nephrotic syndrome

A

proteinuria >3.5 g/d, edema, hyperlipidemia, lipiduria

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4
Q

rapidly progressive GN

A

ARF in days, hematuria, dysmorphic RBC and RBC casts and proteinuria, nephritis

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5
Q

acute renal failure sx

A

oliguria or anuria with azotemia

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6
Q

chronic renal failure sx

A

s/s of uremia (impaired renal excretory function + biochemical and endocrine abnormalities)

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7
Q

focal vs diffuse

A

focal is

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8
Q

segmental vs global

A

segmental is only part of glomerulus

global is all of glomerulus

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9
Q

sclerosis in kidney

A

increased ECM

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10
Q

primary renal causes of nephrotic syndrome

A

minimal change dz
focal segmental
membranous
membranoproliferative

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11
Q

secondary/systemic causes of nephrotic syndrome

A

amyloid
diabetes
SLE

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12
Q

minimal change disease epi

A

m/c nephrotic syndrome in kids, M>F

20% adults with nephrotic syndrome, M=F

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13
Q

minimal change dz pathogenesis

A

aka lipoid nephrosis
unknown cause, a/w recent URI or allergen exposure
? T-cell dysfxn -> lymphokines -> epithelial damage -> loss of charge and size selection -> albuminuria
*Selective loss of LMW proteins

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14
Q

minimal change dz clinical

A

edema and albuminuria with exacerbations and remissions
tx w empirical steroids, biopsy if no response
adults need biopsy to establish cause of nephrotic syndrome

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15
Q

minimal change dz histo

A

LM: normal
IF: normal
EM: fusion of foot processes

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16
Q

minimal change dz tx and prognosis

A

> 90% remit on steroids but recur
may remit spontaneously
few fail to respond to steroids or cytotoxic agents -> renal failure
*consider genetic d/o involving glomerular slit diaphragm (NPHS2 for podocin) if no response

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17
Q

FSGS epi and s/s

A

5-10% nephrotic syndromes in kids, up to 35% in adults (m/c cause)
heavy non-selective proteinuria
may have microscopic hematuria, reduced GFR, HTN

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18
Q

FSGS pathogenesis

A

idiopathic (HIV, heroin, podocin or cytoskeletal mutations), drug-induced, or inherited
may be a/w obesity or systemic dz
? in spectrum with MCD
epithelial cell damage d/t IgM and C3 deposits -> loss of size selectivity and charge

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19
Q

FSGS histo

A

segmental collapse of some glomerular tufts
hyalinosis (eos, PAS+ deposits on endothelial surface of GBM)
hypercellular mesangium with foam cells
adherence to Bowman’s capsule
IF: IgM and C3 in mesangium and subendothelial, thick GM

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20
Q

FSGS prognosis

A

most progress to RF slowly
some respond to steroids or cytotoxics
20% rapid decline -> RF in 2 yrs
25-50% recurrence after transplant

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21
Q

membranous nephropathy epi

A

common cause of nephrotic syndrome in adults 35-40
85% primary (idio) - AI Abs to renal Ags on podocytes (PLA2-R)
2’ d/t circulating immune complexes a/w systemic dz, toxins, drugs, infections, metabolic abnormalities

22
Q

membranous nephropathy clinical and prognosis

A

nephrotic syndrome or proteinuria
50% -> RF in 2-20 yr
25-30% remission
renal vein thrombosis can cause sudden loss of fxn in 25-50% cases

23
Q

membranous nephropathy histo

A

uniform thickening of GBM
no increased cellularity
“spike” projections of GBM to subepi space to surround deposits of IgG and C3

24
Q

chronic glomerulonephritis causes

A 
post-strep
RPGN
membranous
FSGS
MPGN
IgA
others
25
Q

diabetic glomerulosclerosis epi and prevalence

A

occurs in 30-40% type 1 (IDDM) and 20-30% type 2 (NIDDM) patients
m/c cause of ESRD in US
30-40% diabetics develop nephropathy

26
Q

stages of diabetic kidney disease

A

1 - hyperfiltration, inc GFR, microalbuminuria
2 - grossly normal
3 - mild proteinuria, declining GFR, HTN - 10-15 years
4 - heavy proteinuria –> ESRD - 5-7 years

27
Q

diabetic glomerulosclerosis pathogenesis

A

glycosylation of BM > 10 years
hemodynamic factors
systemic and microvascular HTN

28
Q

diabetic glomerulosclerosis histo

A

nodular: Kimmelsteil-Wilson nodules, mesangial nodules
diffuse: uniform GBM thickening, diffuse mesangial sclerosis and proliferation

29
Q

renal amyloid pathogenesis

A

AL (Ig light chain) in plasma cell dyscrasias and idiopathic
AA (serum proteins) in systemic dz
common COD in pts with amyloidosis
amyloid catabolized by mesangial cells, extend into subendothelial space and GBM -> disrupted charge or structure

30
Q

renal amyloid histo

A

amorphous eosinophilic deposits
amyloid in glomeruli, vessels, interstitium
IF: congo red stain with apple-green birefringence

31
Q

glomerulonephritis

A

an inflammatory d/o w focal or diffuse hypercellularity of glomerulus

32
Q

glomerulonephritis pathogenesis

A

circulating immune complexes or in situ formation where Ab binds GBM Ag
alternative complement pathway, ? cell-mediated

33
Q

glomerulonephritis mechanisms

A

immune complexes in mesangium, subendothelium, lamina densa, supepithelial

34
Q

crescentic/ RPGN type 1 causes

A

anti-GBM (5%): idiopathic (20%) and Goodpasture’s

35
Q

crescentic/ RPGN type 2 causes

A

immune complex: idiopathic (25%), post-infectious, SLE, IgA nephropathy/ HSP

36
Q

crescentic/ RPGN type 3 causes

A

pauci-immune: no IC or anti-GBM Abs, ANCA present, ANCA-associated vasculitides, idiopathic (55%)

37
Q

RPGN pathogenesis

A

damage to GBM, fibrin escapes into Bowman’s space

fibrin, MFs, and parietal epithelial cell proliferation form crescents

38
Q

RPGN histo

A

LM: cellular crescents in Bowman’s space
IF: linear pattern with anti-GBM; granular pattern with immune complex
EM: cells and fibrin in crescents, capillary loops broken and collapsed

39
Q

RPGN clinical presentation

A 
fatigue, weakness, malaise
decreased output and hematuria
HTN rare at onset
rapid deterioration into RF
look for signs of systemic dz
40
Q

post-infectious GN

A

nephritic syndrome following URI or skin infection
hematuria, proteinuria, facial edema, HTN
*immune-mediated process

41
Q

post-infectious GN pathogenesis

A

circulating Ag-Ab complexes attach to GBM initiating complement
deposits trapped in subepithelial spaces

42
Q

post-infectious GN histo

A

LM: large hypercellular (infiltrating neutros) glomeruli, subepi deposits may be seen
crescents present = worse prognosis
IF: C3 and IgG deposits on GBM
EM: mesangial proliferation of endothelium and mesangium, “humps” on epithelial surface of GBM

43
Q

membranoproliferative GN epi and clinical

A

children and adolescents
slow progression to RF
clinical: range from mild proteinuria to nephrotic to nephritic

44
Q

membranoproliferative GN types and causes

A

type 1: circulating immune complex or planted antigen

2 (dense deposit dz): autoantibody against C3 convertase (C3 nephritic factor) -> activation of alternative pathway

45
Q

type 1 MPGN histo

A

LM: “tram tracks”, increased cellularity, inc matrix
IF: C3 in coarse granular pattern on GBM and mesangium; C1q, C4, IgG, IgM, properidin may be present
EM: duplication of GBM, subendothelial deposits

46
Q

type 2 MPGN (dense deposit disease) histo

A

LM: dense deposits in diffusely thickened GBM
IF: faint or broken linear C3 along GBM with punctate deposits
EM: e- dense deposits in GBM, Bowman’s capsule, tubular BM

47
Q

IgA nephropathy clinical

A

asymptomatic hematuria or proteinuria
1-2 d post URI and recurrent gross hematuria
nephrotic and nephritic syndromes uncommon
benign, but 20% develop CRF in 10 yrs
*m/c worldwide glomerular dz

48
Q

IgA nephropathy histo

A

LM: varied with inc mesangium
IF: granular mesangial deposits of IgA
EM: deposits in mesangial matrix

49
Q

systemic d/o with significant glomerular involvement

A

SLE, DM, amyloidosis, HSP, bacterial endocarditis, Goodpasture’s, polyateritis, Wegener’s, cryoglobulinemia, myeloma

50
Q

SLE kidney pathology types

A 
1 - normal
2 - mesangial
3 - focal proliferative
4 - diffuse proliferative
5 - membranous
6 - advanced sclerosing
51
Q

Alport syndrome

A

X-linked defect in type 4 collagen
nerve deafness, lens dislocation, cataracts
irregular BM thickening, hematuria

52
Q

Fabry disease

A

a-galactosidase A deficiency
accumulation of ceramide trihexoside
proteinuria

Path 4 (8 decks)

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