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CRRAB II > Renal Pathology Lecture II > Flashcards

Renal Pathology Lecture II Flashcards

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1
Q

Medullary Sponge Kidney

A
  • -Disease of adults
  • -Often incidental finding
  • -Normal kidney function
  • -Multiple cystic dilations of collecting ducts in medulla
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2
Q

Gross features of medullary sponge kidney

A

Dilated papillary ducts in the medulla

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3
Q

Micro features of medullary sponge kidney

A

Cysts lined by cuboidal or transitional epithelium

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4
Q

Dialysis-Associated (acquired) cystic disease

A
  • -Most asymptomatic
  • -Almost always develop cysts with dialysis
  • -7% of dialysis patients will develop renal cell carcinoma within the cysts
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5
Q

Simple cysts

A
  • -Multiple or single (typically cortical)
  • -1-5 cm in size commonly
  • -Filled with clear fluid (ultrafiltrate)
  • -Pretty avascular on CT-angiography
  • -Single layer of cuboidal or flattened epithelium line the cysts
  • -No clinical significance, but will want to differentiate from possible tumor
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6
Q

Glomerulonephritis

A

IMMUNE MEDIATED DISEASE

–Primary or secondary

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7
Q

Histologic patterns of glomerular injury

A
  1. Hypercellularity (increase in glomerular cells, increase in WBCs, formation of crescents)
  2. Basement membrane thickening
  3. Hyalinization and sclerosis
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8
Q

Diffuse

A

All glomerular involved

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9
Q

Focal

A

Proportion of glomeruli involved (less than 50%)

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10
Q

Global

A

Entire single glom involved

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11
Q

Segmental

A

Part of single glom involved

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12
Q

Antibody-mediated injury

A
  • -In situ immune complex deposition (Goodpasture, hemyann, planted antigens)
  • -Circulating immune complex antigen
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13
Q

Immune mechanisms of glomerular injury

A
  1. Antibody-mediated injury
  2. Cell-mediated immune injury
  3. Activation of alt. complement path
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14
Q

Anti-GBM Glomerulonephritis

A
  • -Abs directed against normal parts of GBM
  • -Ab may cross-react w/other basement membranes (such as pulmonary alveoli)
  • -Ag component of type IV collagen!
  • -
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15
Q

Anti-GBM glomerulonephritis appearance on IF

A

Homogenous, linear/ribbon-like appearance. Diffuse.

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16
Q

Membranous nephritis

A
  • -Antigen: M-type Phospholipase A2 receptor
  • -IF: granular and interrupted pattern
  • -EM: electron dense deposits along subepithelial aspect of GBM
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17
Q

“Planted” antigens

A
  • -Non-glomerular origin, but localize in kidney

- -Abs form against them

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18
Q

Circulating immune complex nephritis

A
  • -Glomerular injury from trapping of circulating Ag/Ab complexes within gloms
  • -Type III hypersensitivity
  • -Antigens endogenous (SLE) or exogenous (streptococci)
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19
Q

IF and EM findings with circulating immune complex nephritis

A

IF: granular deposits
EM: electron-dense deposits, mesangial, subepithelial, or subendothelial

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20
Q

Progression in glomerular disease

A

Once reduced to 30-50% of normal, progress to end-stage renal failure no matter what inciting event was

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21
Q

Histological findings in glomerular disease

A
  • -Focal segmental glomerulosclerosis

- Tubulointerstitial fibrosis

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22
Q

Focal segmental glomerulosclerosis as an adaptive change

A
  • -Compensatory hypertrophy occurs
  • -Hemodynamic changes in ind. glomeruli (increases in flow, filtration, transcapillary pressure)
  • -Leads to segmental sclerosis
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23
Q

Treatment of focal segmental glomerulosclerosis

A

Renin-angiotensin inhibitors

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24
Q

Tubulointerstitial fibrosis

A
  • -Develops with glomerulonephritides over time
  • -Ischemic tubules downstream from sclerotic glomeruli
  • -Proteinuria directly toxic to downstream tubular cells
  • -Increased acute and chronic inflammation occurs
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25
Nephritic syndrome
- -INFLAMMATORY process - -Hematuria - -RBC casts in urine - -Azotemia, oliguria, HTN (from salt retention), proteinuria
26
Nephrotic syndrome
- -Massive proteinuria (>3.5g/day) - -Hypoalbuminemia leading to edema - -Hyperlipidemia - -Frothy urine w/fatty casts. - -Podocyte damage disrupting filtration charge barrier. - -Hypercoagulable state
27
Types of nephritic syndrome
- -Acute poststreptococcal glomerulonephritis - -Rapidly progressive (crescenteric) glomerulonephritis (RPGN) - -Diffuse proliferative glomerulonephritis (DPGN) (and nephroltic syndrome) - -IgA nephropathy (Berger Disease) - -Alport syndrome - -Membrano-proliferative glomerulonephritis (MPGN) (often also nephrotic syndrome)
28
Types of nephrotic syndrome
- -Focal segmental glomerulosclerosis - -Minimal change disease (lipoid necrosis) - -Membranous nephropathy - -Amyloidosis - -Diabetic glomerulo-nephropathy
29
Acute poststreptococcal glomerulonephritis general characteristics
- -Occurs 1-4 weeks post-infection of pharynx or skin. - -Resolves spontaneously - -Type III hypersensitivity reaction - -All ages, most common in children
30
Acute poststreptococcal glomerulonephritis lab findings
- -Decreased C3 serum levels - -Seum antistreptolysisin O, antiDNase B titers high - -Red cell casts - -Mild proteinuria
31
Acute poststreptococcal glomerulonephritis LM, IF, and EM findings
- -LM: glomeruli enlarged and hypercellular w/proliferation of endothelial and mesangial cells. Infiltration of neutrophils and monocytes - -IF: Granular IgG, IgM - -EM: sub epithelial immune complex humps
32
What helps make diagnosis for acute poststreptococcal GN
EM
33
Clinical presentation for Acute poststreptococcal GN
- --Nephritic - -"SMOKY URINE" hematuria - -Malaise - -Oliguria - -PERIORIBITAL EDEMA - -Mild HTN - -Adults may have atypical presentation
34
Rapidly progressive (crescentic) GN (RPGN) general info
- -SEVERE injury to glomerulus - -Not caused by specific entity - -Poor prognosis - ->50% of glomeruli will have crescents
35
Crescents
Proliferations of parietal epithelial cells of Bowmans capsule mixed with inflammatory cells
36
Type I RPGN
- -Anti-GBM GN | - -IF show LINEAR deposits of IgG ,C3, in GBM
37
Type II RPGN
- -Immune complex mediated - -IF: GRANULAR pattern, "lumpy-bumpy) - -Seen with PSGN, SLE, IgA nephropathy
38
Type III RPGN
- -Pauci-immune type - -LACK OF IF STAINING - -Most have P or C-ANCA - -Some cases due to vasculitis, most are idiopathic
39
RPGN gross, micro, EM findings
- -Gross: large, pale kidneys w/petechiae - -Micro: crescent formation w/fibrin strands - -EM: ruptures in GBM +/- subepithelial deposits
40
Nephrotic syndrome pathophysiology
- -Increased permeability of GBM to plasma proteins - -Massive proteinuria - -Hypoalbuminemia - -Loss of colloid osmotic pressure and edema - -Increased liver synthesis of lipoproteins - -Infections due to loss of Ig and complement - -Hypercoaguable state due to loss of anticoags
41
Number one cause of nephrotic syndrome in children
Minimal change disease (75% of cases)
42
Most common causes of nephrotic syndrome in adults
Membranous and Focal segmental glomerulosclerosis
43
Membranous GN general info
--Can be primary (idiopathic) or secondary to other conditions (DM, NSAIDs, HBV, HCV, SLE, solid tumors, etc.)
44
Pathogenesis of membranous GN
- -Chronic Ag-Ab mediated disease - -Antigens can be endogenous or exogenous - -Damage to GBM is COMPLEMENT MEDIATED
45
What is often the autoantigen in membranous GN in adults?
Phospholipase A2
46
Microscopic findings of membranous GN
- -Normocellular gloms - -Uniform, diffuse, thickening of capillary wall (capillary loops look like cheerios)!!! - -"Spikes" on silver stain correspond to BM material between deposits - -Deposits become part of very thickened GBM - -Late mesangial sclerosis and glomerular hyalinization occur
47
IF of membranous GN
Granular deposits along GBM--Deposits contain IgG and C3. Nephrotic presentation of SLE
48
EM of membranous GN
--Subepithelial deposits --"Spike and dome" appearance Spikes of BM between deposits --Thickened GBM w/lucent defects (deposits resorbed) --Effacement of foot processes
49
Course of membranous GN
- -Chronic proteinuria and slow deterioration (40% chronic renal insufficiency, 10% die or have renal failure) - -Highly variable! Can't predict who will do well - -Corticosteroids are +/- - -If secondary treat the cause
50
Minimal change disease (Lipid nephrosis) (MCD) general info
- -Most common cause of nephrotic syndrome in children (peak 2-6 yrs old) - -Associated w/atopy, may follow URI or routine immunization - -Increased incidence in Hodgkin lymphoma! - -RESPONDS TO CORTICOSTEROID TREATMENT
51
Pathogenesis of MCD
- -Visceral epithelial cell injury - -T cell dysfunction and release of cytokines - -May lead to loss of charge barrier or adhesion defects between epithelial cells
52
Microscopic findings of MCD
- -Normal glomeruli!! | - -Proximal tubules may be fill with lipid
53
IF findings in MCD
No staining
54
EM findings in MCD
- -DIffuse effacement (cytokine mediated) of foot processes of visceral epithelial cells (podocytes) - -No deposits
55
Clinical course of MCD
- -Massive proteinuria (mostly albumin) - -No renal failure, often no HTN - ->90% of kids respond to corticosterioids - -Can recur - -Adults respond more slowly, still recover - -Damage to visceral epithelial cells reversed by steroid therapy
56
Focal Segmental Glomerulosclerosis (FSGS) general info
- -Sclerosis of some gloms in portion of glomerulus - -Associated with HIV, heroin addiction, sickle cell disease, morbid obesity - -Secondary change in area of previous necrotizing lesion - -Adaptive response to loss of renal tissue - -Currently most common cause of nephrotic syndrome in adults
57
Pathogenesis of FSGS
- -Thought to be related to MCD - -Damage to visceral epithelial cells - -Genetic abnormalities of proteins which localize to slit diaphragm and lead to FSGS
58
LM findings of FSGS
- -Make diagnosis this way - -Focal, need good biopsy - -Collapse of GBM, increased mesangial matrix, hyalinization, +/- foam cells - -Segmental sclerosis and hyalinization
59
EM findings of FSGS
- -Diffuse effacement of foot processes (similar to MCD) | - -Focal detachment of epithelial cells from GBM
60
IF findings of FSGS
Mesangial deposits of IgM and C3 (in sclerotic area)
61
Clinical course in FSGS
- -Doesn't respond well - -Nephrotic syndrome, HTN, reduced GFR - -Poor response to corticosteroids - -At least 50% have ESRD in 10 yrs - -RECURS POST-TRANSPLANTATION - -Worse prognosis with HIV nephropathy
62
HIV nephropathy
- -Most commonly FSGS, collapsing variant - -See cystically dilated tubules filled with proteinaceous material and inflammation - -EM: TUBULORETICULAR INCLUSIONS IN ENDOTHELIAL CELLS - -5-10% of HIV positive patients, more commonly in African-Americans
63
Membranoproliferative GN (MPGN) general info
- -5-10% of nephrotic syndrome in children and young adults. - -May present with nephritic syndrome - -Proliferation of glomerular cells, leukocyte infiltration, changes in GBM
64
Associations w/MPGN
- -Chronic immune complex disease (SLE, Hep B, Hep C, endocarditis, infected ventriculoatrial shunts) - -Partial lipodystrophy (type II) - -Alpha-1 antitrypsin deficiency - -Malignancy (CLL, lymphoma, melanoma)
65
Pathology of MPGN
--Type 1 and 2 distinguished by IF, EM. Microscopic (1 and 2 similar).
66
Microscopic findings of MPGN
- -Large, hypercellular glomeruli w/lobular architecture ("flower-like") - -Thickened GBM - -Silver stain show "tram track" or "double contour" from mesangial cell interposition into GBM
67
Type I MPGN
- -2/3 of cases - -IF: granular C3, IgG, C1q, C4 - -SUBENDOTHELIAL DEPOSITS +/- subepithelial and mesangial deposits
68
Pathogenesis of Type I MPGN
- -Immune complex disease | - -Activation of classic and alternative complement pathways
69
Type II MPGN or dense deposit disease
--IF: granular C3 only EM: DENSE DEPOSIT DISEASE Lamina densa RIBBON-LIKE and extremely dense from deposits --Excess activation of alt complement pathway
70
Clinical course of MPGN
50% develop chronic renal failure in 10 years - -steroids and immunosuppressive drugs not helpful - -COMMONLY RECURS POST-TRANSPLANT
71
IgA nephropathy (Berger disease)
- -Most common type of GN worldwide - -Causes recurrent hematuria w/RBC casts - -+/- proteinuria (can be in nephrotic range) - -HSP systemic disease w/overlapping features - -Associated w/celiac sprue, liver disease
72
Pathogenesis of IgA nephropathy
- -Plasma polymeric IgA increased - -IgA aberrantly glycosylated - -Immune complexes deposit or are formed in mesangium
73
LM of IgA nephropathy
Mesangial proliferation
74
IF of IgA nephropathy
Mesangial deposition of IgA!!! | +/- C3, properdin, IgG, IgM
75
EM of IgA nephropathy
Paramesangial and mesangial immune complex deposits
76
Clinical course of IgA nephropathy
--Hematuria following respiratory, GI, UT infection --Variable course presentation 15-40% develop chronic RF over 20 years --Disease recurs post-transplantation
77
Types of hereditary nephritis
- -Alport Syndrome | - -Thin membrane disease
78
Alport syndrome presentation
- -Nephritis, eye problems, sensorineural deafness - -Most cases X-linked dominant - -Males affected more frequently and severely
79
Alport syndrome pathophysiology
--Mutation in type IV collagen--> thinning and splitting of GBM
80
Alport syndrome microscopic findings
- -Glomeruli w/segmental proliferation or sclerosis - -Mesangial matrix increases - -Persistance of fetal-like glomeruli - -Foam cells
81
EM findings in Alport Syndrome
- -Splitting of the lamina densa - -Changes are widespread - -Diagnosis made based on EM findings
82
Clinical course of Alport Syndrome
- -Present w/hematuria at 5-20 yrs - -+/- proteinuria (Can be nephrotic) - -Renal failure by 20-50
83
Thin membrane disease (Benign familial hematuria)
- -Fairly common - -Present w/hematuria - -EM shows diffuse thinning of GBM - -Abnormal genes encoding collagen chains - -Excellent prognosis but homozygous patients may progress to RF
84
Chronic Glomerulonephritis
- -End result of specific types of GN | - -Some present at end stage w/no antecedent disease
85
Gross and micro findings of Chronic GN
Gross: small, diffusely granular kidneys Micro: globally hyalinized glomeruli (hyaline material contains plasma proteins, mesangial matrix, GBM material, collagen) Atrophy and fibrosis of tubules/interstitium
86
Progression to Chronic GN (in order of those most likely to progress)
1. RPGN (90%) 2. FSGS (50-80%) 3. Membranous (50%) 4. Membranoproliferative (50%) 5. IgA nephropathy (30-50%) 6. Poststreptococcal (1-2%)
87
SLE general info
- -Autoimmune disease | - -Affects skin, joints, kidney, serosal membranes
88
Lupus nephritis
- -60-70% involvement based on LM exam - -Nearly all SLE patients show kidney involvement on IF and EM eval - -5 patterns of involvement
89
IF and EM findings in SLE nephritis
IF: "full house" stains with everything EM: subendothelial and sometimes IgG-based immune complexes often with C3 deposition LM: "WIRE LOOP" LESION (thickening of capillary wall by subendothelial deposits)
90
HSP clinical presentation
Purpuric skin lesions on arms, legs and buttocks, abdominal pain, vomiting, bleeding, arthralgia, renal abnormalities (1/3 of patients) (hematuria, proteinuria/nephrotic syndrome, renal issues worse in adults, may have crescentic GN)
91
Most common age of HSP
3-8 year old after URI
92
HSP pathophysiology in kidneys
IgA deposition in mesangium
93
Diabetic nephropathy general info
- -ESRD in up to 40% of Type I and II DM - -Proteinuria in 50% (typically 12-22 yrs after diagnosis) - -Micro: capillary BM thickening, diffuse mesangial sclerosis, nodular glomerulosclerosiss
94
Pathogenesis of diabetic nephropathy
- -Metabolic defect: increases type IV collagen, fibronectin, nonenzymatic glycosylation of proteins, leads to thickened GBM, increased mesangial matrix - -Hemdynamic effects: increased GFR, glomerular hypertrophy early, leads to glomerulosclerosis
95
Pathology of diabetic nephropathy
- -Capillary basement membrane thickening (see on EM) - -Diffuse mesangial sclerosis - -Nodular glomerulosclerosis
96
Nodular glomerulosclerosis in DM nephropathy
Kimmelstiel-Wilson disease - -Hyaline masses in periphery of glomerulus - -15-30% of DM patients, assoc. w/ RF
97
Clinical course of diabetic nephropathy
- -Microalbuminuria - -HTN - -Diabetic nephropathy - -ESRD - -Treatment options: long-term dialysis, renal transplant, pancreas transplant

CRRAB II (13 decks)

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