Disease of
The urinary system
Department of Pathology and Pathophysiology,
Medical and Life Science College,Jianghan University
Deng Hao,Liu lijiang
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
The kidney is a structurally
complex organ that has
evolved to subserve a number
of important functions,
excretion of the waste
products of metabolism,
regulation of body water and
salt,
maintenance of appropriate
acid balance,
and secretion of a variety of
hormones and autocoids.
The filtering membrane
Fenestrated endothelial cell
Glomerular basement membrane (GBM)
Visceral epithelial cell (podocyte)
Mesangial cell
Glomerular barrier function
3.6 nm radius; 70.000 kD
Size Charge Configuration
The complex structure of the capillary wall
The integrity of the GBM
Anionic moieties present within the GBM
Filtration slit diaphragm of the visceral epithelial cell
A thin layer
of fenestrated
endothelial
cells,each
fenestra being
70 to 100 nm
in diameter.
Fenestrated endothelial cell
A glomerular basement membrane (GBM) with a thick,
electron-dense central layer,the lamina densa,and thinner,
electron-lucent peripheral layers,the lamina rara interna
and lamina rara externa,The GBM consists of collagen
(most type IV),laminin,polyanionic proteoglycans,
fibronectin,and several other glycoproteins.
GBM
The visceral epithelial cells (podocytes),structurally
complex cells that possess interdigitating processes
embedded in and adherent to the lamina rara externa
of the basement membrane,Adjacent foot processes
(pedicels) are separated by 20- to 30-nm-wide filtration
slits,which are briged by a thin diaphragm composed
of nephin.
Podocyte
The entire glomerular tuft is supported by
mesangial cells lying between the capillaries,
Basement membrane-like mesangical matrix forms a
meshwork through which the messangial cells are
scatterd,These cells,of mesenchymal origin are
contractile and are capable of proliferation,of laying
down both matrix and collagen,and of secreting a
number of biologically active mediators,as we shall
see,The mesangium also contains a variable number
of monocytes.
Mesangial cell
MES
EP END
MES
Diseases of the kidney
Glomeruli
Tubules
Interstitium
Blood vessels
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Glomerular Diseases
Primary Glomeruloneohritis
e.g,Cresentic GN
Secondary (Systemic) Diseases
e.g,SLE
Hereditary Disorders
e.g,Alport syndrome
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Experimentally,GN can be readily induced
by antigen-antibody reactions,and glomerular
deposits of immunoglobulins,often with
various components of complement,are found
in more than 70% of patients with GN,Cell-
mediated immune mechanisms also play a role
in certain glomerular diseases.
It is a kind of allergy disease that mainly
damage glomerulus.
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
The antigen is not of glomerular (innocent bystander),
It may be endogenous (SLE),or exogenous (bacterial,
viral,parasitic and spirochetal infection),Sometimes
the inciting antigen is unknown,
Antigen-antibody complexes are formed in situ or in
the circulation and then trapped in the glomeruli,
where they produce injury,in large part through the
binding of complement.
The glomerular lesions usually consist of leukocytic
infiltration into glomeruli and proliferation of
endothelial,mesangial and parietal epithelial cells,
Deposits may be located at more than one site in a
given case.
Size and Charge
Immunofluorescence
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
Anti-GBM nephritis
Heymann nephritis
The nephritis model of rabbits called
Masugi nephritis or nephrotoxic serum
nephritis (foreign)
Linear pattern
sometimes Goodpasture syndrome
1%-5%
Anti-Glomerular Basement Membrane nephritis
Immunofluorescence
This is a model of human membranous GN,
The antigen complex located in the coated pits
of visceral epithelial cells.
Granular pattern
In situ
Planted (cationic molecules)
Heymann nephritis
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
There is increasing evidence that sensitized T cells,
formed during the course of a cell-mediated immune
reaction,can cause glomerular injury,Even when
antibodies are present,T-cell-mediated injury cannot
be excluded,Recent evidence suggests that this may be
the case in some forms of rapidly progressive GN.
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
How does glomerular damage ensue?
Loss of glomerular barrier function (e.g,proteinuria)
Reduction in GFR
Complement-leukocyte-mediated mechanism
Complement-dependent but not neutrophil-dependent injury
Antibody direct cytotoxicity
Others
Almost all mediators of inflammation may contribute to
glomerular injury.
Immune complex
complement
C5a
Neutrophils and monocytes
proteases
GBM degradation
Oxygen-derived free radicals
Cell damage
Arachidonic acid metabolites
Reduction in GFR
Complement-leukocyte-mediated mechanism
Immune complex
complement
C5-C9 lytic component (membrane attack complex)
Epithelial cell
detachment
GBM thichening
Secrete damaging chemical mediators
Up-regulate TGFR
Synthesis of extracellular matrix
Complement-dependent but not neutrophil-dependent injury
Mesangial cell cell
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Hypercellularity
GBM thichening and more mesangial matrix
Inflammatory infiltration and necrosis
Hyalinization and sclerosis
Renal tubule and mesenchymal change
Hypercellularity
GBM thichening
more mesangial matrix
Inflammatory infiltration
Necrosis
Hyalinization and sclerosis
Renal tubule and mesenchymal change
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Acute nephritic syndrome
acute onset,visible hematuria,proteinuria,azotemia,edema,
hypertension
Rapidly progressive glomerulonephritis
loss of renal function in a few days or weeks,active urine
sediment (hematuria,dysmorphic red blood cells,red blood
cell casts),anuria
The nephrotic syndrome
heavy proteinuria more than 3.5g/day,hypoalbuminemia,
severe edema,hyperlipidemia and lipiduria
Asymptomatic hematuria or /and proteinuria
Usually a menifestation of mild glomerular abnormalities
Chronic renal failure
Uremia the end result of all chronic renal diseases
Common way of diagnosis of nephritis
Light microscope
Immunofluorescence
Electron microscope (EMS)
H.E.
Special staining– to assist
PAS,BM,mesangial area
Masson,BM,fiber
Silver staining,BM (subtle change)
Light microscope
Character
PAS
FSG
MASSON
FSG
Silver staining
MGN
Immunofluorescence
Linear pattern
Granular pattern
Type of immune complex
Character
Electron microscope (EMS)
Definite the position of deposition
MGN
EMS
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Lesions
Proliferation of the cells in the glomeruliLeukocytic infiltrate
Injure the capillary walls
Hematuria
GFR
Oliguria
Azotemia
Renin
Hypertension
Fluid retension
Some proteinuria
even edema
Ischemic kidney
THE NEPHRITIC SYNDROME
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Acute Proliferative Glomerulonephritis
PGN
Diffuse proliferative GN (PGN)
Immune complex Endogenous lupus nephritis
Exogenous postinfectious GN
Organism Bacterial streptococcus,pneumococcus,et al
Viral mumps,hepatitis B and C,et al
1 to 4 week pharynx or skin
β-hemolytic streptococcus
PGN
Pathogenesis
Postinfectious GN Poststreptococcal GN
Hypocomplementemia
Granular deposits of IgG
Complement on the GBM
before IgG deposition
PGN
Light microscope
Increased cellularity of nearly all glomeruli
“Proliferative”,diffuse”
Endothelial and mesangial cells
proliferation and swelling
Neutrophilic and monocytic
infiltrate
PGN
PGN
PGN
PGN
Immunofluorescence
PGN
Granular pattern
IgG complement
Cleared over about 2 months
PGN
Electron microscope
PGN
Immune complex subendothelial
intramembranous
often subepithelial,hump”
END
EP RBC
BM
PGN
PGN
Volume↑ mild to moderate
Gross apearance
PGN
Hyperemia of surface
Petechial hemorrhage
PGN
PGN
PGN
Clinical Course
PGN
Onset abrupt
heralded by malaise,a slight fever,nausea,and
the nephritic syndrome
Oliguria,azotemia and hypertension
only mild to moderate
Hematuria
smoky brown rather than bright red
Proteinuria
occasionally be severe enough to produce the
nephrotic syndrome
Serum antistreptolysin O titers are elevated in
poststreptococcal cases
Recovery occurs in most children in epidemic cases,
Some children develop rapidly progressive GN or
chronic renal disease.
The prognosis in sporadic cases is less clear,In adults,
15% to 50% of patients develop end-stage renal disease
over the ensuing few years or 1 to 2 decades,In children
is much lower.
Clinical Course
PGN
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Rapidly Progressive Glomerulonephritis
RPGN
Rapidly progressive glomerulonephritis (RPGN)
Clinical syndrome not a specific etiologic form of GN
Rapid and progressive loss of renal function association
with severe oliguria and (if untreated) death from renal
failure within weeks to months.
Crescentic GN parietal epithelial cell
monocyte macrophage
Pathogenesis
Caused by a number of different diseases
No single mechanism can explain all cases
TypeⅠ CrGN
TypeⅡ CrGN
TypeⅢ CrGN
Immunological injury
RPGN
TypeⅠ CrGN
RPGN
Anti-GBM
Characterized by linear deposits of IgG or C3
Goodpasture syndrome
Anti-GBM antibodies are present in the serum
and are helpful in diagnosis.
It is important to recognize typeⅠ CrGN,because
these patients benefit from plasmapheresis.
Type Ⅱ CrGN
RPGN
Immune complex-mediated disorder
Any of the immune complex nephritides
e.g,poststreptococcal GN,SLE,et al
Characterized by granular deposits
Can not be helped by plasmapheresis
Type Ⅲ CrGN
RPGN
Pauci-immune type CrGN
Serum
Antineutrophil cytoplasm antibodies (ANCA)
Lack of anti-GBM antibody or immune complexes
Light microscope
Cresent
Cellular
Fibrous-cellular
Fibrous (scarring)
Proliferation of parietal cells
Migration of monocytes
Fibrin strands
Collagen fibers
RPGN
RPGN
RPGN
RPGN
RPGN
RPGN
RPGN
Immunofluorescence
Granular pattern
Linear pattern
Nothing
RPGN
RPGN
RPGN
Electron microscope
Distinct ruptures in the GBM
Subepithelial deposites in some cases
RPGN
RPGN
Enlarged
Petechial hemorrhage
Gross apearance
pale
RPGN
RPGN
RPGN
RPGN
Clinical Course
Onset
like nephritic syndrome
Oliguria azotemia more pronounced
Proteinuria
sometimes approaching nephrotic range
RPGN
Anuric
requir long-term dialysis or transplantation
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
IgA Nephropathy (Berger Disease)
IgA GN
IgA nephropathy is one of the most common causes
of reccurrent microscopic or gross hematuria and is
the most common glomerular disease worldwide.
Children young adults
Loin pain
several days
subside
recur
every few months
gross hematuria
1 to 2 days
nonspecific upper
respiratory tract infection
Pathogenesis
Deposition of IgA in the mesangium
Abnormality in IgA production and clearance
IgA main immunoglobulin in mucosal
secretions,is at low levels in normal serum
but incresed in 50% of patients with IgA
nephropathy.
IgA GN
Morphology
Vary considerably
Normal
Mesangial widening
Segmental inflammation
IgA GN
Diffuse mesangial proliferation
Overt CrGN rarely
Characteristic picture is of mensangial deposition of IgA
Immunofluorescence
EM electron-dense deposites in the mesangium
IgA GN
IgA GN
IgA GN
Clinical Course
>50% gross hematuria Infection of the
respiratory or,less commonly,gastrointestinal or
urinary tract
5~10% typical acute nephritic syndrome
30~40% Microscopic hematuria with or without
Proteinuria
Maintain normal renal function decades
Chronic renal failure 25% to 50% 20 years
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Lesions
Structural or physicochemical alterations of barrier
Permeability increase
Injure the capillary walls
proteinuria
Hypoalbuminemia Hyperlipidemia
THE NEPHROTIC SYNDROME
Lipiduria
Synthesis of lipoprotein
Reversed albumin-globulin ratio
THE NEPHROTIC SYNDROME
The relative frequencies of the several causes of the
nephrotic syndrome vary according to age.
Children <15 Caused by a lesion primary to the
kidney
Adult Often associated with a systemic
disease
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Minimal Change Disease (Lipoid Nephrosis)
Relatively benign disorder Most frequent cause Children
Normal apearence glomeruli light microscope
Loss of podocyte foot processes electron microscope
Most common between 2 to 3 years any age
Minimal Change Disease
Pathogenesis
Minimal Change Disease
Not clear
Disorder of T cells
Mutation in the nephrin gene
Morphology
Minimal Change Disease
Light microscope
Glomeruli normal
Cells proximal convoluted tubule
heavily laden with lipids
Electron microscope
Lipoid nephrosis
Uniform and diffuse
Loss of the foot processes of the podecytes
reversible
Minimal Change Disease
Minimal Change Disease
Minimal Change Disease
Minimal Change Disease
Clinical Course
Minimal Change Disease
Loss smaller serum proteins
chiefly albumin(selective proteinuria)
>90% respond to a short course of corticosteroid
proteinuria recurs >2/3
some steroid dependent
differentiated from other nonresponders
<5% chronic renal failure after 25 years
Children prognosis good
Adult prognosis worse
therapy response slower relapse more common
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Membranous Glomerulonephritis (MGN)
Membranous Nephropathy
30-50 years
Early
glomeruli normal
Well-developed
diffuse thichening of the capillary wall
MGN
Subepithelial deposite along GBM
Immune complex
complement
C5-C9 lytic component (membrane attack complex)
Epithelial cell
detachment
GBM thichening
Secrete damaging chemical mediators
Up-regulate TGFR
Synthesis of extracellular matrix
Complement-dependent but not neutrophil-dependent injury
Mesangial cell cell
MGN
Pathogenesis
MGN
Chronic immune complex nephritis
Endogenous in situ HLA locus
Exogenous planted
Infection e.g,hepatitis
Malignant tumor e.g,carcinoma of colon
SLE
Inorganic salt e.g,gold
Drug e.g.nonsteroidal anti-inflammatory agents
Morphology
Light microscope
Diffuse thickening of the GBM
MGN
Glomeruli sclerosed hyalinizedFinally
Immunofluorescence microscope
Granular deposition
Immunoglobulin and complement
along the GBM
Normal GBM
MGN
MGN
GBM thickening
MGN
MGN
MGN
MGN
Electron microscope
Spikelike protrusion
Deposite Incorporating into the GBM Disappear
CavityFilled by GBM-like materialThichen
Morphology
MGN
Podocyte lose foot processes
MGN
MGN
MGN
MGN
Clinical Course
Nonselective proteinuria
Corticosteroid nonresponders
>60 proteinuria persists
About 40% renal failure after 2 to 20 years
10~30% partial or complete remission of proteinuria
MGN
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Focal Segmental Glomerulosclerosis (FSG)
10% of all nephrotic syndrome
Children distinguish from minimal change disease
hematuria hypertension proteinuria nonselective
Response to corticosteroid therapy is poor
FSG
Sclerosis some but not all glomeruli
only segment of each glomeruli
50% end-stage renal failure in 10 years
Adult worse than children
Pathogenesis
FSG
Unknown
Injury visceral epithelial cells
circulating mediator
Light microscope
Sclerosis
Focal All levers of the cortex
Immunofluorescence microscope
IgG complement
in the areas of hyalinosis
Segment Global sclerosis
mesangial matrix
collapsed basement membranes
hyalinemasses lipid droplet
Morphology
FSG
FSG
FSG
FSG
Electron microscope
Greater degree of epithelial cell detachment
with denudation of the underlying GBM
Morphology
Podocyte lose foot processes
FSG
Clinical Course
Minimal Change Disease
Progression to renal failure occurs at varying
rates,and about 50% of patients suffer renal
failure after 10 years.
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Membranoproliferative Glomerulonephritis
MPGN
Alterations basement membrane and mesangium
Proliferation glomerular cells
5-10% idiopathic nephrotic syndrome
in children and adults
Nephrotic-nephritic picture
Some proteinuria in the non-nephrotic range
and hematuria
MPGNⅠ and Ⅱ
Light microscope
Morphology
MPGN
Glomeruli large lobular appearance
proliferation of mesangial cells
infiltrating leukocytes
Capillary wall double contour appearance
inclusion within GBM of processes of mesangial
Both types are similar
MPGN
MPGN
Morphology
MPGN
MPGNⅠ and Ⅱ
have different ultratructural and immunofluorescence
MPGNⅠ
subendothelial electron-dense
C3,IgG and
early complement componenets(C1q and C4)
granular pattern
MPGN
MPGN
MPGN
Morphology
MPGN
MPGNⅠ and Ⅱ
have different ultratructural and immunofluorescence
MPGN Ⅱ
subendothelial and lamina densa electron-dense
C3
irregular,ribbon-like electron-dense structure
MPGN
MPGN
MPGN
MPGN
Clinical Course
MPGN
50% Nephrotic syndrome
Some acute nephritis or mild proteinuria
50% < 10 years renal failure
Type Ⅱ disease has a worse prognosis
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Mesangial Proliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
Common China and Asia-Pacific area
Diffuse proliferation mesangial cells
Mesangial matrix
IgG C3 (China); IgM C3; C3
electron-dense deposites in the mesangium
Mesangial Proliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
It probably represents the end stage of a variety of
entities,prominent among which are RPGN,FEG,
MGN and MPGN,
It has been estimated that perhaps 20% of cases
arise with no history of symptomatic renal disease,
Although it may develop at any age,it is usually
first noted in young and middle-aged adults.
Glomeruli hyalinization
fibrosis
Tubules Atrophy
Parenchymal Interstitial fibrosis
Others glomeruli compensation
Tubules Expansion
CHRONIC GLOMERULONEPHRITIS
Lesion
Light microscope
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
Glomeruli hyalinization
fibrosis
Tubules Atrophy
Parenchymal Interstitial fibrosis
Others glomeruli compensation
Tubules Expansion
Lesion
Contracted
Granular
Cortex thin
Small loss weight
White
Gross apearance
CHRONIC GLOMERULONEPHRITIS
Secondary granular atrophy of the kidney
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
Glomeruli hyalinization
fibrosis
Tubules Atrophy
Parenchymal Interstitial fibrosis
Others glomeruli compensation
Tubules Expansion
Lesion
Polyuria
Nocturia
Low gravity uria
Hypertension
Anemia
Renin
Erythropoietin
Uremia
Azotemia
Reabsorption
CHRONIC GLOMERULONEPHRITIS
Clinical Course
Edema
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Pyelonephritis
Pyelonephritis
A group of inflammatory diseases of the kidneys
that involve the renal pelvis,interstitium and
tubules,The glomeruli may be spared altogether or
affected only late in the course.
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
A common suppurative inflammation of the renal
pelvis,interstitium and tubules,is caused by
bacterial infection.
Escherichia coli the most common one
Two routes of bacteria reaching the kidneys
Bloodstream (hematogenous)
Lower urinary tract (ascending infection) Common
Acute Pyelonephritis
Morphology
Acute Pyelonephritis
Gross appearance
Abscesses surface
Widely scattered limited single large
Light microscope
Suppurative necrosis
Abscess
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Clinical Course
Acute Pyelonephritis
Onset sudden
Chills fever malaise
Bladder and urethral irritation
Pyuria bacteriuria
No longer one week
Bacteriuria may persisit much long
Recurrent or Chronic
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Renal Cell Carcinoma
Renal Cell Carcinoma
Derived from the renal tubular epithelium
80~85% primary malignant tumors of the kidney
60~70
40% die
2~3% all cancers in adults
2 men:women
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Morphology
Renal Cell Carcinoma
Clear cell renal carcinoma
Papillary carcinoma
Chromophobe renal carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
谢 谢 大 家！
The urinary system
Department of Pathology and Pathophysiology,
Medical and Life Science College,Jianghan University
Deng Hao,Liu lijiang
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
The kidney is a structurally
complex organ that has
evolved to subserve a number
of important functions,
excretion of the waste
products of metabolism,
regulation of body water and
salt,
maintenance of appropriate
acid balance,
and secretion of a variety of
hormones and autocoids.
The filtering membrane
Fenestrated endothelial cell
Glomerular basement membrane (GBM)
Visceral epithelial cell (podocyte)
Mesangial cell
Glomerular barrier function
3.6 nm radius; 70.000 kD
Size Charge Configuration
The complex structure of the capillary wall
The integrity of the GBM
Anionic moieties present within the GBM
Filtration slit diaphragm of the visceral epithelial cell
A thin layer
of fenestrated
endothelial
cells,each
fenestra being
70 to 100 nm
in diameter.
Fenestrated endothelial cell
A glomerular basement membrane (GBM) with a thick,
electron-dense central layer,the lamina densa,and thinner,
electron-lucent peripheral layers,the lamina rara interna
and lamina rara externa,The GBM consists of collagen
(most type IV),laminin,polyanionic proteoglycans,
fibronectin,and several other glycoproteins.
GBM
The visceral epithelial cells (podocytes),structurally
complex cells that possess interdigitating processes
embedded in and adherent to the lamina rara externa
of the basement membrane,Adjacent foot processes
(pedicels) are separated by 20- to 30-nm-wide filtration
slits,which are briged by a thin diaphragm composed
of nephin.
Podocyte
The entire glomerular tuft is supported by
mesangial cells lying between the capillaries,
Basement membrane-like mesangical matrix forms a
meshwork through which the messangial cells are
scatterd,These cells,of mesenchymal origin are
contractile and are capable of proliferation,of laying
down both matrix and collagen,and of secreting a
number of biologically active mediators,as we shall
see,The mesangium also contains a variable number
of monocytes.
Mesangial cell
MES
EP END
MES
Diseases of the kidney
Glomeruli
Tubules
Interstitium
Blood vessels
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Glomerular Diseases
Primary Glomeruloneohritis
e.g,Cresentic GN
Secondary (Systemic) Diseases
e.g,SLE
Hereditary Disorders
e.g,Alport syndrome
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Experimentally,GN can be readily induced
by antigen-antibody reactions,and glomerular
deposits of immunoglobulins,often with
various components of complement,are found
in more than 70% of patients with GN,Cell-
mediated immune mechanisms also play a role
in certain glomerular diseases.
It is a kind of allergy disease that mainly
damage glomerulus.
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
The antigen is not of glomerular (innocent bystander),
It may be endogenous (SLE),or exogenous (bacterial,
viral,parasitic and spirochetal infection),Sometimes
the inciting antigen is unknown,
Antigen-antibody complexes are formed in situ or in
the circulation and then trapped in the glomeruli,
where they produce injury,in large part through the
binding of complement.
The glomerular lesions usually consist of leukocytic
infiltration into glomeruli and proliferation of
endothelial,mesangial and parietal epithelial cells,
Deposits may be located at more than one site in a
given case.
Size and Charge
Immunofluorescence
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
Anti-GBM nephritis
Heymann nephritis
The nephritis model of rabbits called
Masugi nephritis or nephrotoxic serum
nephritis (foreign)
Linear pattern
sometimes Goodpasture syndrome
1%-5%
Anti-Glomerular Basement Membrane nephritis
Immunofluorescence
This is a model of human membranous GN,
The antigen complex located in the coated pits
of visceral epithelial cells.
Granular pattern
In situ
Planted (cationic molecules)
Heymann nephritis
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
There is increasing evidence that sensitized T cells,
formed during the course of a cell-mediated immune
reaction,can cause glomerular injury,Even when
antibodies are present,T-cell-mediated injury cannot
be excluded,Recent evidence suggests that this may be
the case in some forms of rapidly progressive GN.
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
How does glomerular damage ensue?
Loss of glomerular barrier function (e.g,proteinuria)
Reduction in GFR
Complement-leukocyte-mediated mechanism
Complement-dependent but not neutrophil-dependent injury
Antibody direct cytotoxicity
Others
Almost all mediators of inflammation may contribute to
glomerular injury.
Immune complex
complement
C5a
Neutrophils and monocytes
proteases
GBM degradation
Oxygen-derived free radicals
Cell damage
Arachidonic acid metabolites
Reduction in GFR
Complement-leukocyte-mediated mechanism
Immune complex
complement
C5-C9 lytic component (membrane attack complex)
Epithelial cell
detachment
GBM thichening
Secrete damaging chemical mediators
Up-regulate TGFR
Synthesis of extracellular matrix
Complement-dependent but not neutrophil-dependent injury
Mesangial cell cell
Circulating immune complex
Immune complex in situ
Cell-mediated immune
Mediators of immune injury
Other mechanisms
Pathogenesis
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Hypercellularity
GBM thichening and more mesangial matrix
Inflammatory infiltration and necrosis
Hyalinization and sclerosis
Renal tubule and mesenchymal change
Hypercellularity
GBM thichening
more mesangial matrix
Inflammatory infiltration
Necrosis
Hyalinization and sclerosis
Renal tubule and mesenchymal change
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
Acute nephritic syndrome
acute onset,visible hematuria,proteinuria,azotemia,edema,
hypertension
Rapidly progressive glomerulonephritis
loss of renal function in a few days or weeks,active urine
sediment (hematuria,dysmorphic red blood cells,red blood
cell casts),anuria
The nephrotic syndrome
heavy proteinuria more than 3.5g/day,hypoalbuminemia,
severe edema,hyperlipidemia and lipiduria
Asymptomatic hematuria or /and proteinuria
Usually a menifestation of mild glomerular abnormalities
Chronic renal failure
Uremia the end result of all chronic renal diseases
Common way of diagnosis of nephritis
Light microscope
Immunofluorescence
Electron microscope (EMS)
H.E.
Special staining– to assist
PAS,BM,mesangial area
Masson,BM,fiber
Silver staining,BM (subtle change)
Light microscope
Character
PAS
FSG
MASSON
FSG
Silver staining
MGN
Immunofluorescence
Linear pattern
Granular pattern
Type of immune complex
Character
Electron microscope (EMS)
Definite the position of deposition
MGN
EMS
Pathogenesis
Basic pathological change
Clinical situation
Classification and pathological change
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Lesions
Proliferation of the cells in the glomeruliLeukocytic infiltrate
Injure the capillary walls
Hematuria
GFR
Oliguria
Azotemia
Renin
Hypertension
Fluid retension
Some proteinuria
even edema
Ischemic kidney
THE NEPHRITIC SYNDROME
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Acute Proliferative Glomerulonephritis
PGN
Diffuse proliferative GN (PGN)
Immune complex Endogenous lupus nephritis
Exogenous postinfectious GN
Organism Bacterial streptococcus,pneumococcus,et al
Viral mumps,hepatitis B and C,et al
1 to 4 week pharynx or skin
β-hemolytic streptococcus
PGN
Pathogenesis
Postinfectious GN Poststreptococcal GN
Hypocomplementemia
Granular deposits of IgG
Complement on the GBM
before IgG deposition
PGN
Light microscope
Increased cellularity of nearly all glomeruli
“Proliferative”,diffuse”
Endothelial and mesangial cells
proliferation and swelling
Neutrophilic and monocytic
infiltrate
PGN
PGN
PGN
PGN
Immunofluorescence
PGN
Granular pattern
IgG complement
Cleared over about 2 months
PGN
Electron microscope
PGN
Immune complex subendothelial
intramembranous
often subepithelial,hump”
END
EP RBC
BM
PGN
PGN
Volume↑ mild to moderate
Gross apearance
PGN
Hyperemia of surface
Petechial hemorrhage
PGN
PGN
PGN
Clinical Course
PGN
Onset abrupt
heralded by malaise,a slight fever,nausea,and
the nephritic syndrome
Oliguria,azotemia and hypertension
only mild to moderate
Hematuria
smoky brown rather than bright red
Proteinuria
occasionally be severe enough to produce the
nephrotic syndrome
Serum antistreptolysin O titers are elevated in
poststreptococcal cases
Recovery occurs in most children in epidemic cases,
Some children develop rapidly progressive GN or
chronic renal disease.
The prognosis in sporadic cases is less clear,In adults,
15% to 50% of patients develop end-stage renal disease
over the ensuing few years or 1 to 2 decades,In children
is much lower.
Clinical Course
PGN
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Rapidly Progressive Glomerulonephritis
RPGN
Rapidly progressive glomerulonephritis (RPGN)
Clinical syndrome not a specific etiologic form of GN
Rapid and progressive loss of renal function association
with severe oliguria and (if untreated) death from renal
failure within weeks to months.
Crescentic GN parietal epithelial cell
monocyte macrophage
Pathogenesis
Caused by a number of different diseases
No single mechanism can explain all cases
TypeⅠ CrGN
TypeⅡ CrGN
TypeⅢ CrGN
Immunological injury
RPGN
TypeⅠ CrGN
RPGN
Anti-GBM
Characterized by linear deposits of IgG or C3
Goodpasture syndrome
Anti-GBM antibodies are present in the serum
and are helpful in diagnosis.
It is important to recognize typeⅠ CrGN,because
these patients benefit from plasmapheresis.
Type Ⅱ CrGN
RPGN
Immune complex-mediated disorder
Any of the immune complex nephritides
e.g,poststreptococcal GN,SLE,et al
Characterized by granular deposits
Can not be helped by plasmapheresis
Type Ⅲ CrGN
RPGN
Pauci-immune type CrGN
Serum
Antineutrophil cytoplasm antibodies (ANCA)
Lack of anti-GBM antibody or immune complexes
Light microscope
Cresent
Cellular
Fibrous-cellular
Fibrous (scarring)
Proliferation of parietal cells
Migration of monocytes
Fibrin strands
Collagen fibers
RPGN
RPGN
RPGN
RPGN
RPGN
RPGN
RPGN
Immunofluorescence
Granular pattern
Linear pattern
Nothing
RPGN
RPGN
RPGN
Electron microscope
Distinct ruptures in the GBM
Subepithelial deposites in some cases
RPGN
RPGN
Enlarged
Petechial hemorrhage
Gross apearance
pale
RPGN
RPGN
RPGN
RPGN
Clinical Course
Onset
like nephritic syndrome
Oliguria azotemia more pronounced
Proteinuria
sometimes approaching nephrotic range
RPGN
Anuric
requir long-term dialysis or transplantation
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
IgA Nephropathy (Berger Disease)
IgA GN
IgA nephropathy is one of the most common causes
of reccurrent microscopic or gross hematuria and is
the most common glomerular disease worldwide.
Children young adults
Loin pain
several days
subside
recur
every few months
gross hematuria
1 to 2 days
nonspecific upper
respiratory tract infection
Pathogenesis
Deposition of IgA in the mesangium
Abnormality in IgA production and clearance
IgA main immunoglobulin in mucosal
secretions,is at low levels in normal serum
but incresed in 50% of patients with IgA
nephropathy.
IgA GN
Morphology
Vary considerably
Normal
Mesangial widening
Segmental inflammation
IgA GN
Diffuse mesangial proliferation
Overt CrGN rarely
Characteristic picture is of mensangial deposition of IgA
Immunofluorescence
EM electron-dense deposites in the mesangium
IgA GN
IgA GN
IgA GN
Clinical Course
>50% gross hematuria Infection of the
respiratory or,less commonly,gastrointestinal or
urinary tract
5~10% typical acute nephritic syndrome
30~40% Microscopic hematuria with or without
Proteinuria
Maintain normal renal function decades
Chronic renal failure 25% to 50% 20 years
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Lesions
Structural or physicochemical alterations of barrier
Permeability increase
Injure the capillary walls
proteinuria
Hypoalbuminemia Hyperlipidemia
THE NEPHROTIC SYNDROME
Lipiduria
Synthesis of lipoprotein
Reversed albumin-globulin ratio
THE NEPHROTIC SYNDROME
The relative frequencies of the several causes of the
nephrotic syndrome vary according to age.
Children <15 Caused by a lesion primary to the
kidney
Adult Often associated with a systemic
disease
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Minimal Change Disease (Lipoid Nephrosis)
Relatively benign disorder Most frequent cause Children
Normal apearence glomeruli light microscope
Loss of podocyte foot processes electron microscope
Most common between 2 to 3 years any age
Minimal Change Disease
Pathogenesis
Minimal Change Disease
Not clear
Disorder of T cells
Mutation in the nephrin gene
Morphology
Minimal Change Disease
Light microscope
Glomeruli normal
Cells proximal convoluted tubule
heavily laden with lipids
Electron microscope
Lipoid nephrosis
Uniform and diffuse
Loss of the foot processes of the podecytes
reversible
Minimal Change Disease
Minimal Change Disease
Minimal Change Disease
Minimal Change Disease
Clinical Course
Minimal Change Disease
Loss smaller serum proteins
chiefly albumin(selective proteinuria)
>90% respond to a short course of corticosteroid
proteinuria recurs >2/3
some steroid dependent
differentiated from other nonresponders
<5% chronic renal failure after 25 years
Children prognosis good
Adult prognosis worse
therapy response slower relapse more common
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Membranous Glomerulonephritis (MGN)
Membranous Nephropathy
30-50 years
Early
glomeruli normal
Well-developed
diffuse thichening of the capillary wall
MGN
Subepithelial deposite along GBM
Immune complex
complement
C5-C9 lytic component (membrane attack complex)
Epithelial cell
detachment
GBM thichening
Secrete damaging chemical mediators
Up-regulate TGFR
Synthesis of extracellular matrix
Complement-dependent but not neutrophil-dependent injury
Mesangial cell cell
MGN
Pathogenesis
MGN
Chronic immune complex nephritis
Endogenous in situ HLA locus
Exogenous planted
Infection e.g,hepatitis
Malignant tumor e.g,carcinoma of colon
SLE
Inorganic salt e.g,gold
Drug e.g.nonsteroidal anti-inflammatory agents
Morphology
Light microscope
Diffuse thickening of the GBM
MGN
Glomeruli sclerosed hyalinizedFinally
Immunofluorescence microscope
Granular deposition
Immunoglobulin and complement
along the GBM
Normal GBM
MGN
MGN
GBM thickening
MGN
MGN
MGN
MGN
Electron microscope
Spikelike protrusion
Deposite Incorporating into the GBM Disappear
CavityFilled by GBM-like materialThichen
Morphology
MGN
Podocyte lose foot processes
MGN
MGN
MGN
MGN
Clinical Course
Nonselective proteinuria
Corticosteroid nonresponders
>60 proteinuria persists
About 40% renal failure after 2 to 20 years
10~30% partial or complete remission of proteinuria
MGN
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Focal Segmental Glomerulosclerosis (FSG)
10% of all nephrotic syndrome
Children distinguish from minimal change disease
hematuria hypertension proteinuria nonselective
Response to corticosteroid therapy is poor
FSG
Sclerosis some but not all glomeruli
only segment of each glomeruli
50% end-stage renal failure in 10 years
Adult worse than children
Pathogenesis
FSG
Unknown
Injury visceral epithelial cells
circulating mediator
Light microscope
Sclerosis
Focal All levers of the cortex
Immunofluorescence microscope
IgG complement
in the areas of hyalinosis
Segment Global sclerosis
mesangial matrix
collapsed basement membranes
hyalinemasses lipid droplet
Morphology
FSG
FSG
FSG
FSG
Electron microscope
Greater degree of epithelial cell detachment
with denudation of the underlying GBM
Morphology
Podocyte lose foot processes
FSG
Clinical Course
Minimal Change Disease
Progression to renal failure occurs at varying
rates,and about 50% of patients suffer renal
failure after 10 years.
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Membranoproliferative Glomerulonephritis
MPGN
Alterations basement membrane and mesangium
Proliferation glomerular cells
5-10% idiopathic nephrotic syndrome
in children and adults
Nephrotic-nephritic picture
Some proteinuria in the non-nephrotic range
and hematuria
MPGNⅠ and Ⅱ
Light microscope
Morphology
MPGN
Glomeruli large lobular appearance
proliferation of mesangial cells
infiltrating leukocytes
Capillary wall double contour appearance
inclusion within GBM of processes of mesangial
Both types are similar
MPGN
MPGN
Morphology
MPGN
MPGNⅠ and Ⅱ
have different ultratructural and immunofluorescence
MPGNⅠ
subendothelial electron-dense
C3,IgG and
early complement componenets(C1q and C4)
granular pattern
MPGN
MPGN
MPGN
Morphology
MPGN
MPGNⅠ and Ⅱ
have different ultratructural and immunofluorescence
MPGN Ⅱ
subendothelial and lamina densa electron-dense
C3
irregular,ribbon-like electron-dense structure
MPGN
MPGN
MPGN
MPGN
Clinical Course
MPGN
50% Nephrotic syndrome
Some acute nephritis or mild proteinuria
50% < 10 years renal failure
Type Ⅱ disease has a worse prognosis
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
Mesangial Proliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
Common China and Asia-Pacific area
Diffuse proliferation mesangial cells
Mesangial matrix
IgG C3 (China); IgM C3; C3
electron-dense deposites in the mesangium
Mesangial Proliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
THE NEPHRITIC SYNDROME
Acute Proliferative Glomerulonephritis
Rapidly Progressive Glomerulonephritis
IgA Nephropathy
THE NEPHROTIC SYNDROME
Minimal Change Disease
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
Membranoproliferative Glomerulonephritis
Mesangial Proliferative Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
It probably represents the end stage of a variety of
entities,prominent among which are RPGN,FEG,
MGN and MPGN,
It has been estimated that perhaps 20% of cases
arise with no history of symptomatic renal disease,
Although it may develop at any age,it is usually
first noted in young and middle-aged adults.
Glomeruli hyalinization
fibrosis
Tubules Atrophy
Parenchymal Interstitial fibrosis
Others glomeruli compensation
Tubules Expansion
CHRONIC GLOMERULONEPHRITIS
Lesion
Light microscope
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
Glomeruli hyalinization
fibrosis
Tubules Atrophy
Parenchymal Interstitial fibrosis
Others glomeruli compensation
Tubules Expansion
Lesion
Contracted
Granular
Cortex thin
Small loss weight
White
Gross apearance
CHRONIC GLOMERULONEPHRITIS
Secondary granular atrophy of the kidney
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
CHRONIC GLOMERULONEPHRITIS
Glomeruli hyalinization
fibrosis
Tubules Atrophy
Parenchymal Interstitial fibrosis
Others glomeruli compensation
Tubules Expansion
Lesion
Polyuria
Nocturia
Low gravity uria
Hypertension
Anemia
Renin
Erythropoietin
Uremia
Azotemia
Reabsorption
CHRONIC GLOMERULONEPHRITIS
Clinical Course
Edema
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Pyelonephritis
Pyelonephritis
A group of inflammatory diseases of the kidneys
that involve the renal pelvis,interstitium and
tubules,The glomeruli may be spared altogether or
affected only late in the course.
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
A common suppurative inflammation of the renal
pelvis,interstitium and tubules,is caused by
bacterial infection.
Escherichia coli the most common one
Two routes of bacteria reaching the kidneys
Bloodstream (hematogenous)
Lower urinary tract (ascending infection) Common
Acute Pyelonephritis
Morphology
Acute Pyelonephritis
Gross appearance
Abscesses surface
Widely scattered limited single large
Light microscope
Suppurative necrosis
Abscess
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Acute Pyelonephritis
Clinical Course
Acute Pyelonephritis
Onset sudden
Chills fever malaise
Bladder and urethral irritation
Pyuria bacteriuria
No longer one week
Bacteriuria may persisit much long
Recurrent or Chronic
Acute Pyelonephritis
Chronic Pyeloneohritis
Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Chronic Pyelonephritis
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
Renal Cell Carcinoma
Renal Cell Carcinoma
Derived from the renal tubular epithelium
80~85% primary malignant tumors of the kidney
60~70
40% die
2~3% all cancers in adults
2 men:women
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Morphology
Renal Cell Carcinoma
Clear cell renal carcinoma
Papillary carcinoma
Chromophobe renal carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Renal Cell Carcinoma
Structure of kidney
Glomerulonephritis
Pyelonephritis
Tumors
谢 谢 大 家！
