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Renal Pathology Flashcards

1
Q

Hematuria

A

Blood in the urine
Can by glomerular (nephrologic), hallmark of nephritic syndrome
Or extraglomerular (urologic)

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2
Q

Nephritic Syndrome

A

Clinical entity, usually acute onset

  • Hematuria w/ dysmorphic cells and RBC casts
  • Some degree of oliguria and azotemia
  • Hypertension
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3
Q

Acute Postinfectious Glomerulonephritis

A

Children: Acute Nephritic Syndrome (hematuria, edema, HTN, renal failure)
Adults: Acute Nephritic Syndrome may be less common

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4
Q

Acute Postinfectious Glomerulonephritis

Epidemiology

A

Typically in children 6-10 years
Rarer in adults
Sporadic or endemic

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5
Q

Acute Postinfectious Glomerulonephritis

Etiology

A

1-4 weeks after recovery from infection
Pharynx Group A-B-hemolytic Streptococcal infections (GABHS), nephritogenic, M protein virulence factor
Other infections (pneumo, staph, viral)
Skin (impetigo)

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6
Q

Acute Postinfectious Glomerulonephritis

Pathogenesis

A

Immune complexes form in circulation (antigen + igG)
Deposition of immune complexes in capillary wall of glomerulus
Complement is activated (C5a)
Neutrophils attracted, mediate damage
Endocapillary proliferation and structural damage
“Swiss cheese” appearance with hematuria
Immune complexes are also formed IN-SITU (SUBEPITHELIAL DEPOSITS OR HUMPS) Unique to this syndrome

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7
Q

Acute Postinfectious Glomerulonephritis

Histology

A 
Endocapillary proliferation (hypercellular tuft, capillaries occluded)
neutrophilic infiltration (tri-lobed cells)
Immune complex deposits by immunofluorescence and electron microscopy
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8
Q

Acute Postinfectious Glomerulonephritis

Laboratory Tests

A 
Tea-colored (smokey/coca cola) urine
Hematuria, mild proteinuria
ASO titer INC
Complement levels DEC
Biopsy only required if course is ATYPICAL
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9
Q

Acute Postinfectious Glomerulonephritis

Prognosis

A

Children TOTAL RECOVERY in >95%
Adults have slow progression to chronic glomerulonephritis (because not identified until they go into renal failure)
15-50% of adults develop ESRD
Small subset of children/adults may develop severe acute illness

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10
Q

Acute Postinfectious Glomerulonephritis

Treatment

A

Supportive

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11
Q

IgA Nephropathy (Berger Disease)

A

RECURRENT gross and microscopic hematuria
Episodes of gross hematuria w/in 1-2 days of nonspecific URI (or GI or UTI)
Painless hematuria following infection
Hematuria for days, recurrence every few months
Henoch-Schoenlein purpura (main in children, small vessel vasculitis, purpura on skin, GI)

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12
Q 
IgA Nephropathy (Berger Disease)
Epidemiology
A

IgA nephropathy = most common glomerular disease worldwide

In children and young adults

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13
Q 
IgA Nephropathy (Berger Disease)
Etiology
A

Mucosal (respiratory, GI from food/bacteria) infection leads to IgA production
IgA immune complexes form and deposit in mesangium
Genetic or acquired abnormality in immune regulation
Abnormality in clearance of IgA
Antibodies against abnormally glycoslyated IgA
Activation of complement via alternative (rather than classic) pathway

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14
Q 
IgA Nephropathy (Berger Disease)
Histology
A

Mesangial proliferation (big spots on immunofluorescence)
IgA-complex in mesangium
Electron dense deposits by electron microscopy

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15
Q 
IgA Nephropathy (Berger Disease)
Laboratory Tests
A

Hematuria
Mild proteinuria
Complement levels NORMAL (liver is able to keep up with complement consumption)
Usually need biopsy for diagnosis/prognosis (see how much glomerulus is involved)

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16
Q 
IgA Nephropathy (Berger Disease)
Prognosis
A

Variable -> dependent on glomerular pathology
If prolonged can lead to renal failure
Small proportion of patients get aggressive course

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17
Q 
IgA Nephropathy (Berger Disease)
Treatment
A

Supportive

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18
Q

Hereditary Nephritis

A

Group of inherited glomerular diseases
MUTATIONS in glomerular basement membrane proteins
Structural alteration, error in synthesis of IV collagen (kidney, lens, cochlea)
Alport Syndrome
- nephritis
- nerve deafness
-various eye disorders, early cataracts

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19
Q

Hereditary Nephritis

Typical Clinical Presentation

A

Hearing and ocular abnormalities

Isolated hematuria

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20
Q

Hereditary Nephritis

Epidemiology

A

Age 5-20 at presentation

20-50 years with overt renal failure

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21
Q

Hereditary Nephritis

Etiology

A

X-linked inheritance
(+) family history
Male pts: full spectrum
Female pts: carries, rare with disease (X-chromosome inactivation)

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22
Q

Hereditary Nephritis

Pathology

A

Lamina dense splitting and lamination
“Basket weave”
Is not 3 distanct layers anymore

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23
Q

Hereditary Nephritis

Histology

A

Normal in parrafin sections
NO IMMUNE COMPLEX ( - immunofluoroscopy)
Electron microscopy is diagnostic (basket weave)

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24
Q

Hereditary Nephritis

Laboratory tests

A

Hematuria

Genetic Testing

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25
Hereditary Nephritis | Prognosis
Overt renal failure between 20-50 years of age
26
Hereditary Nephritis | Treatment
Supportive Transplantation Counseling Family Testing (prenatal testing is available)
27
Rapidly progressive glomerulonephritis (RPGN)
Rapidly progressive loss of renal function Nephritis syndrome, gross hematuria Cresents
28
Glomerular cresent
``` Glomerulus turns into a cresent shape Stops bleeding but compressed tuft Decreases filtration Rapid progression to renal failure If there is severe glomerular basement membrane injury, blood and FIBRIN and MACROPHAGES leak into Bowman space, parietal epithelial cells proliferate ```
29
Causes of cresents
Anti-glomerular basement antibody (RPGN type I) Some circulating immune complex glomerulonephritis (RPGN type II) Pauci-immune/ANCA associated (RPGN type III)
30
Rapidly progressive glomerulonephritis (RPGN) Type I
Gross hematuria Drop in urinary output (acute renal failure) Hemoptysis (small capillaries in lung are involved as well) KIDNEY AND LUNG
31
Rapidly progressive glomerulonephritis (RPGN) Type I | Epidemiology
Young men Rare 12% of cresentic glomerulonephritis
32
Rapidly progressive glomerulonephritis (RPGN) Type I | Etiology
Anti-glomerular basement membrane antibodies Exposure of basement membrane: viruses, smoking, solvents (paints, dyes), drugs, industrial exposure Genetic predisposition to autoimmunity
33
Rapidly progressive glomerulonephritis (RPGN) Type I | Histology
Immunofluorescence: Antibody deposited along entire length of glomerular basement membrane Membrane destroyed, multiple areas of necrosis (GROSS HEMATURIA)
34
Goodpasture Syndrome
Antibody cross-reactivity with pulmonary alveolar basement membrane Linear IgG deposits along glomerular and alveolar basement membranes Antigen: noncollagenous protein (NC1) Rapidly progressive glomerulonephritis and hematuria and pulmonary hemorrhage (hemoptysis)
35
Rapidly progressive glomerulonephritis (RPGN) Type I | Pathology
Crescents Linear stain for IgG (not seen by electron microscopy) IgG in glomeruli/pulmonary alveoli
36
Rapidly progressive glomerulonephritis (RPGN) Type I | Laboratory tests
Anti-glomerular basement membrane antibodies in serum | Levels may be low in rapid binding on kidney
37
Rapidly progressive glomerulonephritis (RPGN) Type I | Prognosis
Renal failure | Pulmonary failure
38
Rapidly progressive glomerulonephritis (RPGN) Type I | Treatment
Plasmapharesis | Removal of pathogenic antibodies from the circulation
39
Rapidly progressive glomerulonephritis (RPGN) Type II | Clinical Presentation
Gross hematuria | Drop in urinary output (acute renal failure)
40
Rapidly progressive glomerulonephritis (RPGN) Type II | Epidemiology
Rare 1% of postinfectious, small subset of IgA Systemic lupus erythematosus (SLE) Children, young adults (10-40 yo)
41
Rapidly progressive glomerulonephritis (RPGN) Type II | Etiology
Severe immune complex formation with necrosis | Breaks in glomerular basement membrane
42
Rapidly progressive glomerulonephritis (RPGN) Type II | Pathology
Crescents Immune complexes (IgG+C3; IgA+C3) Electron dense deposits by electron microscopy
43
Rapidly progressive glomerulonephritis (RPGN) Type II | Laboratory tests
Depends on etiology (ie postinfectious, IgA nephropathy, diffuse proliferative lupus) Postinfectious: complement drop and ASO titers IgA: no complement drop SLE: no complement drop Biopsy needs to be done because presentation clinical picture is not specific enough
44
Rapidly progressive glomerulonephritis (RPGN) Type II | Prognosis
Chronic renal failure
45
Rapidly progressive glomerulonephritis (RPGN) Type II | Treatment
Immunosuppression
46
Rapidly progressive glomerulonephritis (RPGN) Type III
ELK (eyes/ears/nose, lungs, kidneys) Drop in urinary output (acute renal failure) Gross hematuria Hemoptysis, SOB
47
Rapidly progressive glomerulonephritis (RPGN) Type III | Epidemiology
Older patients
48
Rapidly progressive glomerulonephritis (RPGN) Type III | Etiology/pathogenesis
Antineutrophil cytoplasmic autoantibodies (ANCA) ANCAs react w/neutrophils causing early degranulation and release of lytic enzymes ANCAs are present in serum DO NOT form circulating immune complexes Direct cause of pauci-immune crescentic glomerulonephritis/systemic vasculitis
49
Rapidly progressive glomerulonephritis (RPGN) Type III | Laboratory Tests
Immunofluorescence on neutrophils: the ANCA shows up | ANCA: test for their presence
50
Rapidly progressive glomerulonephritis (RPGN) Type III | Pathology
Crescents Extraglomerular vasculitis NO immune complex deposits NO electron dense deposity NO anti-glomerular basement membrane autoantibodies Immunofluorescence: negative (pauci immune) Electron microscopy: negative (pauci immune) In routine studies we don't see the offending body, because there are no complexes deposited in kidney
51
Rapidly progressive glomerulonephritis (RPGN) Type III | Prognosis
Renal failure | Pulmonary
52
Rapidly progressive glomerulonephritis (RPGN) Type III | Treatment
Immunosuppression
53
Rapidly progressive glomerulonephritis (RPGN) Type III | Wegener granulomatosis
Vasculitis with necrosis and granuloma-like pathology c-ANCA Ear/nose/throat Lung Kidney (remember Goodpasture is just lung/kidney)
54
Churg-Strauss Snydrome
``` Allergic granulomatosis and angiitis Small vessel necrotizing vasculitis with eosinophils Asthma, alleric rhinitis Lung infiltrates Peripheral eosinophilia Extravascular necrotizing granulomas Palpable purpura GI bleeding Renal disease myocardial infiltrates p-ANCA ```
55
Recap: | Type I RPGN
Anti glomerular basement membrane autoantibodies Children Goodpasture Antibody against collagen in glomerular and alveolar basement membrane Hematuria + hemoptysis Young adult male
56
Recap: | Type II RPGN
``` Circulating immune complex Young adults Post-strep, diffuse proliferative glomerulonephritis Diffuse immune complex deposition Usually subendothelial Most common in lupus ```
57
Recap: | Type III RPGN
``` Pauci immune/ANCA Elderly Wegener granulomatosis (c-ANCA) Microscopic angiitis (p-ANCA) Churg-Strauss (p-ANCA) Eosinophils and asthma in Churg-Strauss ```
58
Nephrotic Syndrome
Increased permeability to plasma proteins Membrane becomes more porous to proteins (not RBCs) Massive proteinuria > 3.5 g daily Hypoalbuminemia
59
Membranous Nephropathy | Clinical Presentation
Edema (looks like CHF in elderly) Thrombosis (loss of ATIII) Infections 10% in SLE pts
60
Membranous Nephropathy | Epidemiology
Young/middle age adults between 30 and 60 30% adults, second most common nephrotic syndrome 5% in children 85% autoimmune (idiopathic), 15% secondary
61
Membranous Nephropathy | Etiology
In-situ subepithelial immune complex formation Autoimmune response against renal antigen Carcinomas (lung, colon, breast, kidney), leukemia, non-Hodgkin's lymphoma Infections: malaria, hep B and C, congenital syphilis, leprosy Drugs: penicillamine, gold
62
Membranous Nephropathy | Pathogenesis
``` In-situ immune complex formation Antibody against glomerular antigens IgG + complement granular deposits Rxn on basal surface of podocytes Injury to podocytes, loss of slit diaphragms Foot process effacement NO cellular rxn (no proliferation/WBCs) NO INFLAMMATORY RESPONSE ```
63
Membranous Nephropathy | Histology
No inflammation, no proliferation Electron microscopy: subepithelial deposits Immunofluorescence: granular deposits of IgG and C3 Silver stain: spike and dome (immune complex deposits are silver negative, basement membrane is black) Capillary wall looks thickened and stiffer
64
Membranous Nephropathy | Laboratory Tests
Nephrotic snydrome (hypoalmbuminemia, hyperlipidemia, lipiduria) Secondary hyperlimidemia, inc in total cholesterol Inc in LDL, cholesterol Accelerated atherogenesis NO COMPLEMENT DROP (bc chronic and slowly progressing) Antibody testing for PLA2R NEED TO BIOPSY, clinical presentation is too vague
65
Membranous Nephropathy | Prognosis
1/3 pts will have spontaneous remission 1/3 progress to require dialysis 1/3 continue to have proteinuria, without progression to renal failure
66
Membranous Nephropathy | Treatment
``` Difficult Immunosuppressive drugs (Prednisone) Non-specific anti-proteinuric Secondary: Tx of underlying disease Recurrence after transplantation ```
67
Minimal Change Disease | Clinical Presentation
Edema (periorbital, generalized)
68
Minimal Change Disease | Epidemiology
Children 2-6 yo 65% of nephrotic syndrome in children NO BIOPSY IF UNCOMPLICATED in course Adults, 10% nephrotic syndrome in adults, need biopsy
69
Minimal Change Disease | Etiology
REVERSIBLE podocytes injury T cell derived, ?cytokines Dpression of immunity (viral infections, Hodkin disease) NSAIDs
70
Minimal Change Disease | Pathology
``` No inflammation/cellular proliferation No immune complex deposits Effacement (fusion) of foot processes Membrane becomes thicker but more permeable Reversible (with steroids ```
71
Minimal Change Disease | Histology
Normal paraffin sections No immune complex deposits Foot processes effacement via electron microscopy
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Minimal Change Disease | Laboratory Tests
Nephrotic Syndrome
73
Minimal Change Disease | Prognosis
Several episodes of nephrotic syndrome (relapses) Normal renal function Resolution at puberty
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Minimal Change Disease | Treatment
Steroids
75
Focal and Segmental Glomerular Sclerosis (FSGS) | Clinical Presentation
``` Nephrotic syndrome Higher incidence of hematuria Reduced GFR HTN Non-selective proteinuria (albumin only) ```
76
Focal and Segmental Glomerular Sclerosis (FSGS) | Epidemiology
Adults 35%, most frequent pathology in human biopsy Children 10%, older children African American Hispanic
77
Focal and Segmental Glomerular Sclerosis (FSGS) | Etiology
IRREVERSIBLE injury to podocytes
78
Focal and Segmental Glomerular Sclerosis (FSGS) | Histology
Some normal glomeruli Some focal (segmental) obliteration (sclerosis) of glomerular capillaries Collapse of capillary loops, increase in mesangial matrix Immunofluorescence: negative Electron microscopy: effacement of epithelial foot processes in ALL GLOMERULI
79
Focal and Segmental Glomerular Sclerosis (FSGS) | Progression
``` Initially only rare glomeruli involved (focal) Preferentially juxtamedullary glomeruli With progression more glomeruli involved Global sclerosis Tubular atrophy, interstitial fibrosis ```
80
Focal and Segmental Glomerular Sclerosis (FSGS) | Pathology
Segmental obliteration (sclerosis) of capillaries Collapse of capillary loops Inc. mesangial matrix Initially only rare glomeruli involved (focal)
81
Focal and Segmental Glomerular Sclerosis (FSGS) | Laboratory Tests
Nephtrotic syndrome | Genetic testing
82
Focal and Segmental Glomerular Sclerosis (FSGS) | Prognosis
Progression to renal failure
83
Focal and Segmental Glomerular Sclerosis (FSGS) | Treatment
Initially steroid responsive Progressively steroid dependent/resistant Recurrence in transplants
84
Focal and Segmental Glomerular Sclerosis (FSGS) | Genetics
Inherited mutations in genes encoding slit diaphragm proteins Genetic risk allels in APL1 in AA, adult-onset Can be diagnosed in very young childnren
85
Focal and Segmental Glomerular Sclerosis (FSGS) | HIV varient
Collapse of tuft + proliferation of visceral epithelial cells Normally podocytes cannot proliferate HIV induces dedifferentiation, restores their ability to proliferate Progression is rapid/dramatic, aggressive form Morphology looks different Wrinkled/collapsed
86
``` Membranoproliferative Glomerulonephritis (MPGN) Clinical Presentation ```
Nephrotic syndrome and hematuria
87
``` Membranoproliferative Glomerulonephritis (MPGN) Epidemiology ```
``` Older children (10%) Adults (10%) ```
88
``` Membranoproliferative Glomerulonephritis (MPGN) Etiology ```
Immune complex formation Classical complex activation Secondary: chronic autoimmune disorders, hepatitis, endocarditis, chronic bacterial infections Monoclonal proteins (aka paraproteins) produced by clonal B cells/plasma
89
``` Membranoproliferative Glomerulonephritis (MPGN) Pathology ```
Thicken glomerular basement membrane "Double contour"or "tram track" on silver stain IgG + complement deposits, subendothelial Increase in mesangial cells (chase immune complexes into walls) Lobular tufts Thicke glomerular basement
90
``` Membranoproliferative Glomerulonephritis (MPGN) Laboratory Tests ```
Low complement
91
``` Membranoproliferative Glomerulonephritis (MPGN) Prognosis ```
Progression to renal failure
92
``` Membranoproliferative Glomerulonephritis (MPGN) Treatment ```
Treat underlying disease (endocarditis, hepatitis, etc)
93
Dense Deposit Disease | Clinical Presentation
Nephrotic syndrome with hematuria
94
Dense Deposit Disease | Epidemiology
Rare | Older children
95
Dense Deposit Disease | Etiology
Sustained activation of complement via alternative pathway (non-antibody mediated) No antigen-antibody formation
96
Dense Deposit Disease | Pathology
Complement (C3) C3 convertase is usually digested quickly, but if something that prevents its removal the cascade keeps going No immunoglobulin Dense deposits within lamina densa (seen via electron microscopy)
97
Dense Deposit Disease | Laboratory Tests
Complement levels | Molecular studies
98
Dense Deposit Disease | Prognosis
Poor Progression to renal failure Recurrence in transplants
99
Dense Deposit Disease | Treatment
New therapies controlling complement activation
100
Diabetic nephropathy
Glomerular lesions Diffuse and nodular glomerular sclerosis + nephritic syndrome Atherosclerosis and arteriosclerosis Pyelonephritis (acute & chronic) Nonenzymatic glycosylation of vascular basement membrane resulting in hyaline arteriosclerosis
101
Amyloidoses
``` Deposits of anormally folded protein Congo red positive Plasma cell dyscrasia/multiple myeloma Kidney involvement: nephrotic syndrome FAT biopsy for screening! Tx depends on protein type Survival improves with early diagnsis ```
102
SLE
Systemic lupus erythematosus Multisystem, renal involvement with edema Primarily young women Immune DNA-antiDNA complexes Proliferative glomerulonephritis with necrosis and cresents Nephritic syndrome 10% develop nephrotic syndrome Do kidney biopsy for staging Tests: autoantibodies, ANAs, anti-sm, anti-dsDNA
103
Ischemic ATI
Acute Tubule Injury BP drop Severe trauma Acute pancreatitis
104
Toxic ATI
``` Acute Tubule Injury Drugs (antibiotics) Contrast dyes Poisons Organic solvents ```
105
Combine ATI
``` Acute Tubule Injury Ischemic + nephrotoxic Mismatched blood transfusion/other hemolytic crises (hemoglobinuria) Skeletal muscle injury (myoglobinuria) Intratubular casts Crystals Interstitial components ```
106
1st Degree Tubulo-interstitial Nephritis
Renal tubules and interstitium Infections, acute and chronic Drugs & toxins Other (metabolic: urate, oxalate, hypercalcemia, neoplasm: multiple myeloma)
107
2nd Degree Tubulo-interstitial Nephritis
Associated with other diseases Glomerulonephritis Autoimmune
108
Acute Pyelonephritis
Bacterial infection (E. coli, proteus, klebsiella, enterobacter, streptococcus faecalis) Also fungi and viruses Can come via blood (hematogenous) Or ASCENDING up the ureters
109
Acute- Drug Induced Interstitial Nephritis
Not Dose related IgE mediate + skin test to drug hapten Delayed hypersensitivity rxn (type IV)
110
NSAIDs Nephritis
Acute hypersensitivity interstitial nephritis Nephrotic syndrome + renal failure Looks like minimal change disease (foot processes effacement) BUT WE START SEEING CREATINE IN URINE Renal failure
111
Pronephros
4th week
112
Mesonephros
Caudally Tubules degenerate Duct persists Mesonephric duct comes in contact with cloaca, grows cranially as ureteric bud
113
Renal Dysplasia
Aberrant nephronic differentiation NOT NEOPLASIA Presence of immature elements: undifferentiated mesenchyme, cartilage Grossly enlarged kidneys, irregular shape (bunch of grapes)
114
Potter's Sydrome
Fetal urine production is important for amniotic fluid development Without amniotic fluid lungs develop poorly Small, deformed, hypoplastic lungs
115
Autosomal Recessive Polycystic Kidney Disease (ARPKD)
``` Rare PKHD1 gene Enlarged kidneys Sponge-like appearance Dilated/elongated tubules Liver has cysts as well, fibrosis ```
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Adult Polycystic Kidney Disease
``` Pain, colic, mass, hemorrhage, hematuria, renal failure, HTN Common Autosomal DOMINANT Cysts in kidney and liver Tx is transplantation Intracranial berry aneurysms Mitral valve prolapse ```
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Aquired Cystic Disease
Dialysis associated Cortical and medullary cysts Renal cell carcinoma can occur
118
Benign Kidney Tumors
Oncocytoma (distal nephron, mahogeny brown with central scar) Angiomyolipoma (vessels/smooth muscle/fat, huge/irregular vessels
119
Renal Cell Carcinoma
TRIAD: COSTO-VERTEBRAL PAIN, MASS, HEMATURIA Incidentally discovered Cause paraneoplastic syndromes (often how its discovered) Found in the elderly Very deadly Can be sporadic or genetic Kinda looks like adrenal gland Extremely chemo-resistant, there are targeted therapies
120
von Hippel-Lindau (VHL) syndrome
``` Sutosomal dominant 37 years Multiple bilateral cysts and tumors, high vascularity Angiomas of retina Hemangioblastoma (CNS/cerebellum/spine) Pheos in some ```
121
Urothelial Carcinoma
Adults Renal pelvis, ureter, frequently with bladder cancer Hematuria ANALGESIC NEPHROPATHY is a risk factor
122
Wilm's tumor
25% have other developmental abnormalities WAGR: Wilms tumor, Aniridia, Gu malformation, mental Retardation Peds, most common kidney tumor Malginant blastema (small blue cells, undifferentiated), tubules, stroma Soft tumors, need to be careful when removing Good prognosis Very chemosensitive

MHD (34 decks)

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