Jan11 M2,3-Pathology of glomerular diseases and renal tubules Flashcards
1
Q
give 5 primary glomerular diseases
A
- membranous nephropathy
- MCD
- FSGS
- IgA nephropathy
- Membranoproliferative GN
2
Q
give 5 secondary or systemic diseases that affect the kidney (glomerulus)
A
- DM
- amyloidosis
- SLE
- drugs (NSAIDs)
- infectious (HIV, hepB,C, syphilis)
- malignancy + paraneoplastic
3
Q
4 clinical presentations for glomerular disease
A
hematuria, proteinuria, mixed, renal failure
4
Q
how to know if hematuria is due to a glomerular disease (and not something more downstream)
A
if glomerular disease, RBC casts present
5
Q
RBC casts point to what syndrome
A
nephritic. no RBC casts in nephrotic syndrome
6
Q
pure nephrotic is caused by what
A
problem in glomerular filtration barrier (GBM or other)
7
Q
proteinuria qt in nephrotic
A
3-3.5g a day or more
8
Q
2 types of proteinurias in nephrotic + def
A
selective: albumin only
non-selective: albumin + other prots too
9
Q
5 charact of nephrotic syndrome (labs)
A
- heavy proteinuria (3g a day)
- hypoalbuminemia
- hyperlipidemia
- lipiduria
- edema
10
Q
nephrotic syndrome: urine sediment findings
A
- protein cast/waxy cast
- fatty casts
- oval fat bodies (desquamated tubular cells filled with reabsorbed lipids)
- RBCs but no cast
11
Q
can you find RBCs in nephrotic syndrome urine sediment
A
yes but no RBC casts
12
Q
nephrotic syndrome: 3 main primary diseases
A
- MCD
- FSGS
- membranous nephropathy
13
Q
nephrotic syndrome: 3 main secondary diseases/conditions that can cause it
A
- DM
- amyloidosis
- pregnancy
14
Q
nephrotic syndromes (2 primary and 2 secondary) that present with hematuria
A
primary: 1. membrano-proliferative GN 2. IgA nephropathy
secondary: 1. lupus nephritis 2. Henoch-Schonlein purprue (HSP)
15
Q
most common PRIMARY nephrotic syndrome disease in children and most common PRIMARY in adult
A
children: MCD
adults: FSGS
16
Q
most common SECONDARY nephrotic syndrome diseases in adults
A
- DM
- amyloidosis
- SLE
17
Q
MCD: proteinuria type and only thing seen on biopsy
A
selective
only see effacement of foot processes on EM (LM and IF negative)
18
Q
MCD treatment
A
steroids
19
Q
MCD recurrence and prognosis
A
2/3 recurrence
very good prognosis
20
Q
patho characteristics seen in some nephritic but not nephrotic syndrome
A
crescents, proliferation, hypercell, necrosis, inflammation
21
Q
why selective proteinuria in MCD (2)
A
swelling of podocytes and podocyte fusion = loss of negative charge
22
Q
general pathological feature of DM
A
deposition of glycosylated molecules on BMs everywhere
23
Q
pathophgy of FSGS
A
injury (toxic or immune or genetic) to podocytes and loss of negative charge (hematuria is non selective)
24
Q
main causes of FSGS (cause of podocyte toxicity)
A
HIV, heroin, hyperfiltration (high BP), medication
25
what type of immune toxicity to podocytes in FSGS
immune dysregulation with cytokines/T cells but no immune complexes and no autoimmune rx
26
prognosis of FSGS
50% dev ESRD in 10 yrs
27
type of proteinuria in FSGS and hematuria or not
non-selective proteinuria.
| hematuria is mild or moderate
28
FSGS (focal segmental glomerulosclerosis): sclerosis meaning
scarring (fibrosis). less 50% glomeruli and part of glomeruli
29
why is there a vicious circle in FSGS
hyperfiltration injury. more P in GCs that still function so hyperfiltration injury in the glomerulus and sclerosis of nephrons
30
FSGS sometimes associated with ____
htn
31
membranous nephropathy: pathogenesis
antibodies recognize self protein on glomerular epithelial cells (podocytes)
32
membranous nephropathy: antibody often present (antibody against what)
antibody against PLA2R (podocyte antigen phospholipase A2 receptor)
33
membranous nephropathy: how fast it progresses + prognosis
slowly
| 40% progress to renal failure
34
membranous nephropathy: usual primary cause
a pathology of the GBM (membranous nephropathy is a form of GN)
35
membranous nephropathy: usual secondary causes (4)
- infections (hep, syph, mal)
- cancer
- autoimmune (SLE)
- drugs,toxins
36
FSGS: LM, IF and EM findings
LM: sclerosis + loss of capillaries
EM: non specific deposits of IGM and C3 segmentally
EM: effacement of foot processes
37
membranous nephropathy: LM, IF and EM
LM: diffuse thickening of the glomerular capillary walls
IF: IgG granular along the GBM
EM: sub-epithelial deposits, spikes
38
Diabetic nephrotic syndrome: at what point is it nephrotic syndrome
when proteinuria goes beyond the usual diabetic proteinuria
39
diabetic nephrotic syndrome LM, IF and EM
LM: diffuse or nodular GS, increased mesengium (KW lesions), arteriosclerosis, arteriolosclerosis, hyalinosis
IF: non specific
EM: thickening of GBM
40
Kimmelstiel-Wilson (KW) lesions in what condition and what is it
diabetic nephrotic syndrome
| mesengial matrix increase and mesengial nodules
41
proteinuria and pregnancy usually sign of what
hypertension/pre-eclampsia
42
which nephrotic syndrome diseases (primary and 2ndary) get a biopsy and which do not
```
MCD: no
FSGS: yes
MN: yes
DM: no (or ?)
pregnancy: no
```
43
azotemia and uremia def
azotemia: high BUN
urea: high blood urea
44
nephritic syndrome typical findings (like the 5 of nephrotic but for nephritic)
hematuria, RBC casts, proteinuria, renal failure (azotemia), htn
45
3 most common primary nephritic syndrome diseases (primary GNs) + 1 that we have to remember
- acute post-infectious GN
- IgA nephropathy
- membrano proliferative GN (MPGN)
- RPGN
46
4 most common secondary nephritic syndrome diseases
- lupus nephritis
- Henoch-Schonlein purpura (HSP)
- anti-GBM (Goodpasture syndrome)
- Vasculitis/ANCA related GN
47
acute post infectious GN affects what pop typically
children
48
acute post infectious GN: after what infections usually
beta hymolytic streptococcal infections or URT or skin.
| other: staph, pneumococcus, viruses
49
presentation in acute post infectious GN
tea/cola colored urine, RBC casts, proteinuria, hematuria
50
acute post infectious GN: LM if ever take a biopsy (2-3 things)
diffuse global hypercellularity (prolif of glomerular cells) and infiltration of PMN leukocytes (exudative GN) (+ crescents sometimes)
51
acute post infectious GN on IF if ever take a biopsy
large granular deposits
| C3 and IgG along GBM specifically
52
how IgG deposits in membranous nephropathy (or membranous GN) and acute post infectious GN differ
in MN, smaller deposits and look like a stream
| in acute post infectious GN, granular and larger (but deposit on GBM in both cases)
53
prognosis and dev to ESRD in acute post infectious GN
good prognosis
children mostly affected and 1% children ESRD
adults (rarely): but 15-50% ESRD
54
labs in acute post infectious GN (2)
- low C3 (bc massive deposition in the kidney
| - positive ASOT (for strep infection)
55
IgA nephropathy (Berger): when does it happen and who is affected
1-2 days after URTI
| children and young adults
56
IgA nephropathy (Berger): prognosis
25% ESRD in 10 yrs
57
fix things (2) that are common to all IgA nephropathy (Berger) patients on biopsy
- mesengial prolif
| - IgA deposition on mesengium (IF)
58
variable features of pathophgy of IgA nephropathy (Berger)
highly variable in inflammation, crescents, necrosis and scarring
59
Henoch-Schonlein purpura (HSP) def
systemic form of IgA nephropathy with vasculitis
60
Henoch-Schonlein purpura (HSP) presentation
gross hematuria, GI symptoms, palpable purpura (vasculitis)
61
Henoch-Schonlein purpura (HSP) special thing about the biopsy + finding
can do it on the skin
| find vasculitis with IgA deposits
62
Henoch-Schonlein purpura (HSP) prognosis
even better than IgA nephropathy
63
RPGN presentation
hematuria, htn, RBC casts, oliguria
64
RPGN cause
no cause, it's a syndrome/clinical presentation
65
RPGN main feature
crescents on biopsy
66
RPGN often associated with what cause
-lupus
-anti-GBM
-etc
or sometimes idiopathic
67
treatment of RPGN
corticosteroids
68
RPGN prognosis
(IF UNTREATED), death from renal failure in weeks to months
69
crescents in acute vs chronic RPGN
acute: cellular crescent
chronic: fibrous crescent
70
RPGN biopsy findings
inflam, necrosis, damage to GBM, proinflam mediators make the cells proliferate
71
T/F: crescents are the cause of damage in RPGN
false. leakage of blood and prot
72
3 main types of crescentic GNs
1. anti-GBM
2. immune complex mediated (SLE, IgA nephritis, MPGN, post-infectious
3. pauci-immune (ANCA-related)
73
anti-GBM: pathophgy
antibodies to the type IV collagen (NC1 domain of alpha 3 chain) in the GBM
74
anti-GBM: when is called Goodpasture syndrome
when lung involvement too (type IV collagen also in the lungs)
75
anti-GBM treatment
steroids and plasmapheresis
76
anti-GBM labs
anti-GBM antibodies
77
anti-GBM prognosis
WITH treatment, 60% ESRD
78
anti-GBM: LM, IF and EM
LM: crescents and necrosis
IF: linear IgG deposits on GBM
EM: no deposits visible
79
pauci-immune GN: what population + prognosis
older patients. with treatment, 30% reach ESRD in less than 2 years
80
pauci-immune GN labs
ANCA (anti neutrophil cytoplasmic antibody)
81
pauci-immune GN: LM, IF, EM
LM: crescents
EM: no deposits
IF: no deposits (or minimal)
82
pauci-immune GN: amunt of immune involvement
small
83
any disease with Ab-Ag immune complex deposition can lead to ________
give 3 examples of diseases
RPGN
| lupus, IgA nephropathy, anti-GBM
84
glomerular diseases with crescents (3)
- immune mediated ones (APIGN, MPGN, SLE, IgA nephritis)
- anti-GBM
- ANCA (pauci-immune)
85
glomerular diseases with inflammation involvement (exduate)
APIGN
86
glomerular diseases with scarring (5)
FSGS, diabetes, IGAN (and HSP), RPGN
87
glomerular diseases associated with htn
FSGS, diabetes, RPGN. Nephritic in general. htn = cause of nephrotic in adults
88
glomerular diseases that have hypercellularity (2 main)
APIGN, IGAN (and HSP), RPGN and crescentic diseases
89
what glomerular diseases have necrosis
IGAN (and HSP), anti-GBM
90
what kidney diseases have RBC casts (has to be glomerular bc RBC cast = glomerular)
IgA nephropathy, post-infectious GN, lupus, vasculitis, anti-GBM
(remember cast = nephritic)
91
what kidney diseases have RBC casts (has to be glomerular bc RBC cast = glomerular)
IgA nephropathy, post-infectious GN, lupus, vasculitis, anti-GBM
(remember cast = nephritic)
92
5 tubulointerstitial diseases
- acute pyelonephritis
- chronic pyelonephritis
- reflux nephropathy
- drug induced interstitial nephritis
- ATN (acute tubular injury)
93
acute pyelonephritis cause
bacterial infection (from UTI or form blood)
94
acute pyelonephritis symptoms
sudden onset, malaise, fever, chills, CVA pain, dysuria (painful whne urinate), urgency
95
acute pyelonephritis risk factors
immunosuppresion, women (shorter urehtra), procedures, obstruction, diabetes
96
pathology of acute pyelonephritis
bacterial involvement (one kidney), pus in interstitium, microabcesses and WBC in urine. pus in tubules.
97
papillary necrosis def
form of acute pyelonephritis with ischemic necrosis of the pyramids' papilla in context of diabetes, obstruction, analgesic abuse
98
acute/drug-induced interstitial nephritis: causes
hypersensitivy/allergy/abnormal immune rx/direct toxicity from a medication (antibiotics, analgesics: penicillins, diuretics, NSAIDs)
99
acute/drug-induced interstitial nephritis: symptoms + onset
2-40 days after taking the drug.
| oliguria, azotemia, fever
100
acute/drug-induced interstitial nephritis: UA
hematuria, leukocytes, NO RBC CAST, bit of proteinuria
101
pathology of acute/drug-induced interstitial nephritis
interstitial edema and inflammation
102
ATI/ATN three types
pre-renal, renal, post-renal
103
ATI/ATN is the most common cause of __________
AKI
104
ATI/ATN cause if pre-renal vs if post renal
pre-renal: ischemic damage
| post-renal: obstruction by compression causes toxicity
105
manifestations of ATI/ATN
oliguria/anuria, drop GFR, electrolyte imbalance, acidosis, fluid overload
106
2 types of injuries to tubules in ATI/ATN
ischemic or toxic
107
most affected tubules in ATI/ATN
PCT
108
ATI/ATN biopsy findings
vacuolization of cytoplasm, apical blebbing, dilation of tubules, nuclear loss, denudation
109
amount of inflammation in ATI/ATN
none
110
diseases with hematuria
nephritic + acute pyelonephritis
