Chapter 10
Urinary System
Tang Xiping
Contents
?Glomerulonephritis
?Pyelonephritis
?Tumors of the kidney and
bladder
Questions
? How many patterns can
inflammation be classified into?
? Which three patterns?
? What kind of inflammations
are glomerulonephritis and
pyelonephrits?
[structure]
kidney
ureter
bladder
urethra
Nephron
Glomerulus
tubule
Vascular
pole
Urinary
pole
Capillary
loops
Renal
saccule
Mesangium
Normal Structure of glomerulus
正
常
肾
小
球
Bowman’s
space
Capi,
loops
PodocytesGBM
Fenestrated
capillary
Glomerular filtering membrane
[Function]
1,Form and discharge urine
? Excretes the waste
? Regulates water and salt
? Maintains acid balance
2,Excrete hormone：
Renin
—to regulate blood pressure
Erythropoietin
—to generate RBC
1,25-dihydroxycholecalciferol
—to absorb calcium
Segment 1
Glomerulonephritis (GN)
All are proliferative and most are
immunologically mediated.
Proliferation
of
Epithelial cells
Mesangial cells
Endothelial cells
Two
forms
Immune
Complex
Nephritis in
situ
Circulating
Immune
Complex
Nephritis
[Pathogenesis]
1,Immune Complex
Nephritis In Situ
1) Anti-GBM Nephritis
2) Heymann Nephritis
1） Anti-GBM Nephritis
? Fixed antigens in the glomerular
basement membrane
? Linear continuous pattern of
localization by immunofluorescene
microscopy
肾小球基底膜抗原 连续线形荧光
2） Heymann Nephritis
? ―Planted‖ nonglomerular antigens
? Granular pattern of localization
by immunofluorescene
microscopy
植入性抗原 颗粒状荧光
? The glomerul is an innocent,by
stander”。
The antigen is
not of glomerular origin.
2.Circulating Immune
Complex Nephritis
Endogenous
Exogenous
Unknown
The
origin
颗粒状荧光循环免疫复合物
Three sites
Of
Deposits
In the mesangium
Subendothelial
Subepithelial
3,Cell-Mediated Immune
Glomerulonephritis
Caused by sentisitized T cells.
4,Mediators of immune
injury
Antibodies
Complements
Neutrophils
Monocytes
Macrophages
Platelets
Resident glomerular cells Fibrin related products
Basic pathologic change
1,Hypercelullarity
2,Thickening of GBM
3,Inflammatary exudation and necrosis
4,Hyaline change and sclerosis
Areas of lesions
Diffuse,affecting all or a majority of
glomeruli
Focal,affecting a few or a part of
glomeruli
Globic,involving the whole glomerulus
Segmental,involving only segments of
each glomerulus
弥
漫
性
病
变
球
性
病
变
局
灶
性
病
变
节
段
性
病
变
Clinical manifestations
? Acute nephritic syndrome
? The nephrotic syndrome
? Asymptomatic hemauria or proteinuria
? Rapidly progressive nephritic syndrome
? Chronic nephritic syndrome
Pathologic Types
1,Acute diffuse proliferative GN
2,Rapidly progressive GN
3,Membranous GN
4,Membranoproliferative GN
5,Focal segmental GN
6,Minimal GN
7,mesangial proliferative GN
8,IgA nephropathy
9,Chronic GN
Acute Diffuse Proliferative
Glomerulonephritis
(Endocapillary proliferative GN)
Location:
Diffuse,affecting almost all
glomeruli of two kidneys
Pathogenesis
Post streptococcal GN( related to a
group A streptococcal infection)
Typical immune complex disease:
?Hypocomplementemia
?Granular deposits of IgG
?Complement on the GBM
Morphology
Macropically:
? Kidneys are enlarged and red。
? Sometimes with petechial hemorrhages
大
红
肾
蚤
咬
肾
LM,1,Proliferation and swelling of
endothelial and mesangial cells
PSGN
Normal
2,Neutrophilic infiltrate
3,Epithelial cell
renal tubules:
? Cellular swelling
? Fatty change
? Hyaline change
? Urinary cylinder
in tubules
Electron microscopy
?The immune complex arrayed often
subepithelial,humps” nestled
against the GBM
?Sometimes subendothreial
or intramembranous
Immune
complex
EM：
Subepithelial
deposits
Immunofluorenscence
? Granular pattern of localization on
the capillary wall
? IgG and complement within
the deposits
Acute nephritic syndrome:
Abrupt hematuria,proteinuria,
cylindruria,oliguria,
hypertension,edema.
[Clinical course]
Prognosis
?Recovery
?Rapidly progressive
glomerulonephritis
?Chronic nephritis
?<1% renal failure,heart failure,
hypertensive encephalopathy
Rapidly progressive
glomerulonephrits,RPGN
( crecentic glomerulonephritis)
? The presence of crescents in
most of the glomeruli.
Pathogenesis
1,TypeⅠ RPGN,Anti-GBM disease,
linear deposits of IgG and C3 on the
GBM
2,Type Ⅱ RPGN,Immune complex-
mediated disorder
3,Type Ⅲ RPGN,Pauci-immune type
Morphology
Macroscopically:
? The kidneys are enlarged
and pale.
? Often with petechial
hemorrhages
Light microscopy
The formation of crescents:
Necrosis of
capillary wall
The escape of
abundant fibrinogen
into Bowman’s space
Proliferation
of
parietal epithelial cells
Crescents
formed
新
月
体
性
肾
小
球
肾
炎
新
月
体
Early stage：
Parietal epithelial cell +
Monocytes Cellular crescents
Fibrocytes Fibrous - cellular
crescents
Late stage,Fibrous tissue
fibrous crescents
The crescents obliterate Bowman’s
space and compress the glomeruli
细胞性新月体
纤维性新月体
Electron microscope
? Distinct ruptures in the GBM in all
cases,irregularly thickening of GBM
? Subepithelial deposits in some
cases,
Immunofluorenscence
? Linear pattern
? Granular pattern
? Lack of deposits
Rapidly progressive nephritic
syndrome:
Abrupt hematuria,proteinuria,
anuria,oliguria,anaemia,
renal failure
[Clinical course]
Goodpasture syndrome
Pulmonary hemorrhage & GN
[Pathogenesis]
Anti-GBM nephritis,Anti-GBM
antibodies cross-act with basement
membranes of lung aveloli,resulting in
lung and kidney lesions
[Clinical] Emptysis & Rapidly progress
renal failure
肺
出
血
&
肾
小
球
肾
炎
Goodpasture
syndrome:
Membranous Glomerulonephrits
? Basic change,Diffuse thickening
of the GBM
? Slowly progressive disease,
most common between
ages 30-50 years.
Morphology
?Grossly,
Kidneys enlarged and pale,
LM,Thickening of the capillary wall
膜性肾小球肾炎 (HE染色 )
Cap.
壁增
厚
Electron microscope
? Subepithelial deposits that nestle against
the GBM
? Small,spikelike protrusions of GBM
matrix (“spike and dome” pattern)
? Later,the deposits are catabolized,
leaving for a time cavities within the GBM
EM:
免疫
复合
物
钉突
虫蚀状
膜性肾小球肾炎（嗜银染色）
钉突
Immunofluorescence
? Typical granular deposition
of immunoglobulins (IgG) and
complement( C3) along the
GBM
Nephrotic syndrome:
1,Heavy Proteinuria
2,Hyperlipedemia
3,Severe edema
4,Hypoalbuminemia
[Clinical course]
Membranoproliferative
Glomerulonephritis
[Basic change]:
? Alterations in the basement
membrane and mesangium
? Proliferation of glomerular
cells
Morphology
? Proliferation of mesangial cells as
well as infiltrating leukocytes
extending into the peripheral
capillary loops.
LM:
? The capillary loops have
lobular appearance
? The GBM is thickened,and
shows a double contour or
“tramtruck” apperance
双
轨
征
Cap.
管壁
增厚，
管腔
狭窄
膜增生性肾小球肾炎（嗜银染色）
基底膜增厚呈
车轨状
膜
增
生
性
肾
小
球
肾
炎
(
染
色)
HE
Cap.
丛呈
分叶
状
[Electron microscope]:
TypeⅠ, Subendothelial electron-
dense deposits
TypeⅡ, The lamina densa and the
subendothelial space of th GBM are
transformed into an irregular,
ribbon-like,extremely electron-dense
structure — dense deposit disease
膜
性
增
生
性
肾
小
球
肾
炎
右
Ⅱ
型
左
Ⅰ
型
免疫
复合物
? Type Ⅰ, C3 deposited in a granular
pattern and IgG and early complement
components(C1q and C4) are often
present
? Type Ⅱ, C3 is present in irregular
granular-linear foci in the GBM and
mesangium, IgG is usually absent,as
are C1q and C4
Immunofluorescence
Clinical course
The principle mode of
presentation is the nephrotic
syndrome
Chronic Glomerulonephritis
(Diffuse Sclerosing Glomerulonephritis)
? Kidneys symmetrically contracted
? Surface,red-brown and
diffusely granular
大体：
颗
粒
性
固
缩
肾
?
颗 粒 性 固 缩 肾
Light microscope
1,Advanced scarring of glomeruli
and Bowman’s spaces,
Sometimes complete replacement
and hylalinization.
2,Compensatory hypertrophy of
remained nephrons
3,Interstitial fibrosis,lymphocytic
infiltrate
4,Small arteries thick-walled,
with narrowed lumina
慢
性
肾
小
球
肾
炎
玻
璃
样
变
肾
小
球
纤
维
化
慢性肾小球肾炎
玻
璃
样
变
Chronic nephritic syndrome:
1,Diuresis,nocturia,oliguria,auria
2,Hypertensoin
3,Anaemia
4,Azotemia – renal failure
[Clinical course]
Segment 2
Pyelonephritis
[location], Interstitium,renal pelvis,
tubules
[character],Suppurative imflammation
[age],any age, Female,Male = 10:1
[classification],Acute and Chronic
Two
routes
Through the
bloodstream
From the lower
Urinary tract
上
行
性
感
染
肾
输尿管
膀胱
尿道
Pathogenesis
Gram-negative bacteria,
especially E,coli
Acute pyelonephritis,only
one kind of bacteria
Chronic pyelonephritis,
mixed infection
Macroscopically:
?Kidneys enlarged
?Discrete,yellowish,
raised abscess on the
renal surface
Acute pyelonephritis
急性肾盂肾炎：肾表面及切面多发散
在的小化脓灶（大体）
[Light microscope]
? Suppurative inflammation involving renal
pelvis,interstitium and tubules.
?Abscess formation
? Tubules are filled with pus cell and
bacteria
急 性 肾 盂 肾 炎
肾间质化
脓性炎
急
性
肾
盂
肾
炎
肾
小
管
内
充
满
脓
细
胞
1,Fever,chills,leucocytes ↑
2,Flank pain,bladder irritation
(frequency,dysuria,urgency)
3,Pyuria,bacteriuria,hematuria,
cylinduria (white cell cast)
[Clinical course]
Prognosis
?Recovery
? Improper therapy Chronic
pyelonephritis
Complication：
1） Necrosis of renal papillae
2） Pyonephrosis
3） Perinephric abscess
肾
盂
积
脓
Chronic Pyelonephritis
? A chronic tubulointerstitial
inflammantion
? Renal scarring
大体：瘢痕凹陷性固缩肾
瘢痕
凹陷
[Light microscope]:
? Uneven interstitial fibrosis and an
inflammatory inflitration of lymphocytes,
plasma cells,and occasionally neutrophils.
? Tubules show atrophy in some
areas and hypertrophy in others
? Thyroidization (dilated tubules
with colloid casts)
? Chronic inflammation infiltrate
involving the calyceal mucosa
? Some glomeruli may be involved
慢
性
肾
盂
肾
炎
慢 性 肾 盂 肾 炎
肾盂粘膜慢性炎性细胞浸润
慢 性 肾 盂 肾 炎
肾
小
管
管
腔
内
蛋
白
管
型,
似
甲
状
腺
滤
泡
慢 性 肾 盂 肾 炎
肾
小
球
纤
维
化
玻
璃
样
变
管型
1,Dysuria,nocturia,hypertension
2,Azotemia,uraemia
[Clinical course]
Prognosis
? Correct therapy,Incomplete
recovery
? Abroad lesions,Hypertension,
renal failure
? Unilateral serious disease,
Nephrectomy
Class is
over
Segment 3
Tumors of the kidney and
bladder
[structure]
kidney
ureter
bladder
urethra
? Renal cell carcinoma
? Nephroblastoma
? Transitional cell carcinoma of
the bladder
Renal cell carcinoma
? Adenocarcinoma arising from the
renal tubular epithelium
? Represents about 85% of all primary
malignant tumors of the kidney
? Male,Female ＝ 2,1
肾癌 肾癌
肾
癌
肾癌
Grossly:
?Most commonly at the upper pole
?Usually spherical masses
? Cut surface is colorful,yellow-
gray-white marked with areas
of hemorrhage and necrosis
Histologically:
? ―Clear cells‖ type
?,Granular cells‖ type
Intergradations
may
be
found
Classification based on
molecular origin:
1,Clear cell carcinoma
2,Papillary carcinoma
3,Chromophobe cell carcinoma
肾透明细胞癌
The most common type
?Consists of ―clear cells‖
?The tumor cells may cluster in nests,
tubers or cords
1.Clear Cell Carcinoma
2.Papillary Carcinoma
? Tumor cells line like papilla
? Obvious membrane
? Light basophilic cytoplasm
Have a comparatively
good prognosis
3.Chromophobe carcinoma
[Spread]
?1.Local invasion
?2.Metastasis：
? Hematogenous,early happened,
Unusual organs are involved,
such as mouth,larynx,eyepit,
vagina,
? Lymphatic,renal hilum,
paraaorta lymph nodes
1,Hematuria,flank pain and palpable mass
2,Fever,malaise,lose weight
3,Some tumors produce a variety of
hormone-like substance,
Renin hypertension
Hemopoietin polycythemia
Parathormone analog hypercalcemia
[Clinical course]
肾透明细胞癌
Nephroblastoma
( Wilms’ tumor)
? The third most common organ
malignant tumor in children under
the age of 10 years,and the most
common in kidneys,
? Peak incidence is 2-4 years
? Rare cases occur in adults
[Grossly]
? Usually unilateral( about 90%)
? Generally large,spherical masses
with clear boundary
? Cut surface,
?Soft; fish-flesh areas;
?Gray,hyaline cartilaginous tissue;
?Areas of hemorragic necrosis are
common.
Morphology
肾 母 细 胞 瘤
肾
母
细
胞
瘤
Three bases
? Nests and sheets of primitive blastema
? Abortive tubules and abortive glomeruli
consists of primitive epithelial cells
? Mesenchyma； Spindle cells
Histologically:
肾 母 细 胞 瘤
原
始
肾
小
管
原始肾小球
Transitional Cell Carcinoma
(TCC) of the Bladder
[Age] Peak incidence is 50-70 years
[Position] vesical triangle and
lateral wall of the bladder
The most common malignant
tumor in the urinary system
Morphology
? Range from papillary to flat,
noninvasive to invasive,and from
extremely well –differentiated
(grade Ⅰ )to highly anaplastic
aggressive (grade Ⅲ )
cancers,
膀胱癌
LM,TCCⅠ Papillary tumors with slightly
atypical appearing transitional epithelium.
TCCⅡ have irregular papillary component,
obvious atypia
TCC Ⅲ irregular nests,extremely obvious atypia,
pathologic numerous mitoses are often seen,invade
deep to muscular layer
Atypia
Hyper-
plasia Polarity Mitoses
TCC
Ⅰ Slight >7 Slightly abnormal Rare
TCC
Ⅱ Obvious >10 Abnormal Common
TCC
Ⅲ Extremely obvious Prominent Absent Prominent
[Metastasis]
? Lymphatic spread,Local lymph nodes
? Hematogenous spread,occurs later
[Clinical course ]
Painless hematuria
Class is
over
Urinary System
Tang Xiping
Contents
?Glomerulonephritis
?Pyelonephritis
?Tumors of the kidney and
bladder
Questions
? How many patterns can
inflammation be classified into?
? Which three patterns?
? What kind of inflammations
are glomerulonephritis and
pyelonephrits?
[structure]
kidney
ureter
bladder
urethra
Nephron
Glomerulus
tubule
Vascular
pole
Urinary
pole
Capillary
loops
Renal
saccule
Mesangium
Normal Structure of glomerulus
正
常
肾
小
球
Bowman’s
space
Capi,
loops
PodocytesGBM
Fenestrated
capillary
Glomerular filtering membrane
[Function]
1,Form and discharge urine
? Excretes the waste
? Regulates water and salt
? Maintains acid balance
2,Excrete hormone：
Renin
—to regulate blood pressure
Erythropoietin
—to generate RBC
1,25-dihydroxycholecalciferol
—to absorb calcium
Segment 1
Glomerulonephritis (GN)
All are proliferative and most are
immunologically mediated.
Proliferation
of
Epithelial cells
Mesangial cells
Endothelial cells
Two
forms
Immune
Complex
Nephritis in
situ
Circulating
Immune
Complex
Nephritis
[Pathogenesis]
1,Immune Complex
Nephritis In Situ
1) Anti-GBM Nephritis
2) Heymann Nephritis
1） Anti-GBM Nephritis
? Fixed antigens in the glomerular
basement membrane
? Linear continuous pattern of
localization by immunofluorescene
microscopy
肾小球基底膜抗原 连续线形荧光
2） Heymann Nephritis
? ―Planted‖ nonglomerular antigens
? Granular pattern of localization
by immunofluorescene
microscopy
植入性抗原 颗粒状荧光
? The glomerul is an innocent,by
stander”。
The antigen is
not of glomerular origin.
2.Circulating Immune
Complex Nephritis
Endogenous
Exogenous
Unknown
The
origin
颗粒状荧光循环免疫复合物
Three sites
Of
Deposits
In the mesangium
Subendothelial
Subepithelial
3,Cell-Mediated Immune
Glomerulonephritis
Caused by sentisitized T cells.
4,Mediators of immune
injury
Antibodies
Complements
Neutrophils
Monocytes
Macrophages
Platelets
Resident glomerular cells Fibrin related products
Basic pathologic change
1,Hypercelullarity
2,Thickening of GBM
3,Inflammatary exudation and necrosis
4,Hyaline change and sclerosis
Areas of lesions
Diffuse,affecting all or a majority of
glomeruli
Focal,affecting a few or a part of
glomeruli
Globic,involving the whole glomerulus
Segmental,involving only segments of
each glomerulus
弥
漫
性
病
变
球
性
病
变
局
灶
性
病
变
节
段
性
病
变
Clinical manifestations
? Acute nephritic syndrome
? The nephrotic syndrome
? Asymptomatic hemauria or proteinuria
? Rapidly progressive nephritic syndrome
? Chronic nephritic syndrome
Pathologic Types
1,Acute diffuse proliferative GN
2,Rapidly progressive GN
3,Membranous GN
4,Membranoproliferative GN
5,Focal segmental GN
6,Minimal GN
7,mesangial proliferative GN
8,IgA nephropathy
9,Chronic GN
Acute Diffuse Proliferative
Glomerulonephritis
(Endocapillary proliferative GN)
Location:
Diffuse,affecting almost all
glomeruli of two kidneys
Pathogenesis
Post streptococcal GN( related to a
group A streptococcal infection)
Typical immune complex disease:
?Hypocomplementemia
?Granular deposits of IgG
?Complement on the GBM
Morphology
Macropically:
? Kidneys are enlarged and red。
? Sometimes with petechial hemorrhages
大
红
肾
蚤
咬
肾
LM,1,Proliferation and swelling of
endothelial and mesangial cells
PSGN
Normal
2,Neutrophilic infiltrate
3,Epithelial cell
renal tubules:
? Cellular swelling
? Fatty change
? Hyaline change
? Urinary cylinder
in tubules
Electron microscopy
?The immune complex arrayed often
subepithelial,humps” nestled
against the GBM
?Sometimes subendothreial
or intramembranous
Immune
complex
EM：
Subepithelial
deposits
Immunofluorenscence
? Granular pattern of localization on
the capillary wall
? IgG and complement within
the deposits
Acute nephritic syndrome:
Abrupt hematuria,proteinuria,
cylindruria,oliguria,
hypertension,edema.
[Clinical course]
Prognosis
?Recovery
?Rapidly progressive
glomerulonephritis
?Chronic nephritis
?<1% renal failure,heart failure,
hypertensive encephalopathy
Rapidly progressive
glomerulonephrits,RPGN
( crecentic glomerulonephritis)
? The presence of crescents in
most of the glomeruli.
Pathogenesis
1,TypeⅠ RPGN,Anti-GBM disease,
linear deposits of IgG and C3 on the
GBM
2,Type Ⅱ RPGN,Immune complex-
mediated disorder
3,Type Ⅲ RPGN,Pauci-immune type
Morphology
Macroscopically:
? The kidneys are enlarged
and pale.
? Often with petechial
hemorrhages
Light microscopy
The formation of crescents:
Necrosis of
capillary wall
The escape of
abundant fibrinogen
into Bowman’s space
Proliferation
of
parietal epithelial cells
Crescents
formed
新
月
体
性
肾
小
球
肾
炎
新
月
体
Early stage：
Parietal epithelial cell +
Monocytes Cellular crescents
Fibrocytes Fibrous - cellular
crescents
Late stage,Fibrous tissue
fibrous crescents
The crescents obliterate Bowman’s
space and compress the glomeruli
细胞性新月体
纤维性新月体
Electron microscope
? Distinct ruptures in the GBM in all
cases,irregularly thickening of GBM
? Subepithelial deposits in some
cases,
Immunofluorenscence
? Linear pattern
? Granular pattern
? Lack of deposits
Rapidly progressive nephritic
syndrome:
Abrupt hematuria,proteinuria,
anuria,oliguria,anaemia,
renal failure
[Clinical course]
Goodpasture syndrome
Pulmonary hemorrhage & GN
[Pathogenesis]
Anti-GBM nephritis,Anti-GBM
antibodies cross-act with basement
membranes of lung aveloli,resulting in
lung and kidney lesions
[Clinical] Emptysis & Rapidly progress
renal failure
肺
出
血
&
肾
小
球
肾
炎
Goodpasture
syndrome:
Membranous Glomerulonephrits
? Basic change,Diffuse thickening
of the GBM
? Slowly progressive disease,
most common between
ages 30-50 years.
Morphology
?Grossly,
Kidneys enlarged and pale,
LM,Thickening of the capillary wall
膜性肾小球肾炎 (HE染色 )
Cap.
壁增
厚
Electron microscope
? Subepithelial deposits that nestle against
the GBM
? Small,spikelike protrusions of GBM
matrix (“spike and dome” pattern)
? Later,the deposits are catabolized,
leaving for a time cavities within the GBM
EM:
免疫
复合
物
钉突
虫蚀状
膜性肾小球肾炎（嗜银染色）
钉突
Immunofluorescence
? Typical granular deposition
of immunoglobulins (IgG) and
complement( C3) along the
GBM
Nephrotic syndrome:
1,Heavy Proteinuria
2,Hyperlipedemia
3,Severe edema
4,Hypoalbuminemia
[Clinical course]
Membranoproliferative
Glomerulonephritis
[Basic change]:
? Alterations in the basement
membrane and mesangium
? Proliferation of glomerular
cells
Morphology
? Proliferation of mesangial cells as
well as infiltrating leukocytes
extending into the peripheral
capillary loops.
LM:
? The capillary loops have
lobular appearance
? The GBM is thickened,and
shows a double contour or
“tramtruck” apperance
双
轨
征
Cap.
管壁
增厚，
管腔
狭窄
膜增生性肾小球肾炎（嗜银染色）
基底膜增厚呈
车轨状
膜
增
生
性
肾
小
球
肾
炎
(
染
色)
HE
Cap.
丛呈
分叶
状
[Electron microscope]:
TypeⅠ, Subendothelial electron-
dense deposits
TypeⅡ, The lamina densa and the
subendothelial space of th GBM are
transformed into an irregular,
ribbon-like,extremely electron-dense
structure — dense deposit disease
膜
性
增
生
性
肾
小
球
肾
炎
右
Ⅱ
型
左
Ⅰ
型
免疫
复合物
? Type Ⅰ, C3 deposited in a granular
pattern and IgG and early complement
components(C1q and C4) are often
present
? Type Ⅱ, C3 is present in irregular
granular-linear foci in the GBM and
mesangium, IgG is usually absent,as
are C1q and C4
Immunofluorescence
Clinical course
The principle mode of
presentation is the nephrotic
syndrome
Chronic Glomerulonephritis
(Diffuse Sclerosing Glomerulonephritis)
? Kidneys symmetrically contracted
? Surface,red-brown and
diffusely granular
大体：
颗
粒
性
固
缩
肾
?
颗 粒 性 固 缩 肾
Light microscope
1,Advanced scarring of glomeruli
and Bowman’s spaces,
Sometimes complete replacement
and hylalinization.
2,Compensatory hypertrophy of
remained nephrons
3,Interstitial fibrosis,lymphocytic
infiltrate
4,Small arteries thick-walled,
with narrowed lumina
慢
性
肾
小
球
肾
炎
玻
璃
样
变
肾
小
球
纤
维
化
慢性肾小球肾炎
玻
璃
样
变
Chronic nephritic syndrome:
1,Diuresis,nocturia,oliguria,auria
2,Hypertensoin
3,Anaemia
4,Azotemia – renal failure
[Clinical course]
Segment 2
Pyelonephritis
[location], Interstitium,renal pelvis,
tubules
[character],Suppurative imflammation
[age],any age, Female,Male = 10:1
[classification],Acute and Chronic
Two
routes
Through the
bloodstream
From the lower
Urinary tract
上
行
性
感
染
肾
输尿管
膀胱
尿道
Pathogenesis
Gram-negative bacteria,
especially E,coli
Acute pyelonephritis,only
one kind of bacteria
Chronic pyelonephritis,
mixed infection
Macroscopically:
?Kidneys enlarged
?Discrete,yellowish,
raised abscess on the
renal surface
Acute pyelonephritis
急性肾盂肾炎：肾表面及切面多发散
在的小化脓灶（大体）
[Light microscope]
? Suppurative inflammation involving renal
pelvis,interstitium and tubules.
?Abscess formation
? Tubules are filled with pus cell and
bacteria
急 性 肾 盂 肾 炎
肾间质化
脓性炎
急
性
肾
盂
肾
炎
肾
小
管
内
充
满
脓
细
胞
1,Fever,chills,leucocytes ↑
2,Flank pain,bladder irritation
(frequency,dysuria,urgency)
3,Pyuria,bacteriuria,hematuria,
cylinduria (white cell cast)
[Clinical course]
Prognosis
?Recovery
? Improper therapy Chronic
pyelonephritis
Complication：
1） Necrosis of renal papillae
2） Pyonephrosis
3） Perinephric abscess
肾
盂
积
脓
Chronic Pyelonephritis
? A chronic tubulointerstitial
inflammantion
? Renal scarring
大体：瘢痕凹陷性固缩肾
瘢痕
凹陷
[Light microscope]:
? Uneven interstitial fibrosis and an
inflammatory inflitration of lymphocytes,
plasma cells,and occasionally neutrophils.
? Tubules show atrophy in some
areas and hypertrophy in others
? Thyroidization (dilated tubules
with colloid casts)
? Chronic inflammation infiltrate
involving the calyceal mucosa
? Some glomeruli may be involved
慢
性
肾
盂
肾
炎
慢 性 肾 盂 肾 炎
肾盂粘膜慢性炎性细胞浸润
慢 性 肾 盂 肾 炎
肾
小
管
管
腔
内
蛋
白
管
型,
似
甲
状
腺
滤
泡
慢 性 肾 盂 肾 炎
肾
小
球
纤
维
化
玻
璃
样
变
管型
1,Dysuria,nocturia,hypertension
2,Azotemia,uraemia
[Clinical course]
Prognosis
? Correct therapy,Incomplete
recovery
? Abroad lesions,Hypertension,
renal failure
? Unilateral serious disease,
Nephrectomy
Class is
over
Segment 3
Tumors of the kidney and
bladder
[structure]
kidney
ureter
bladder
urethra
? Renal cell carcinoma
? Nephroblastoma
? Transitional cell carcinoma of
the bladder
Renal cell carcinoma
? Adenocarcinoma arising from the
renal tubular epithelium
? Represents about 85% of all primary
malignant tumors of the kidney
? Male,Female ＝ 2,1
肾癌 肾癌
肾
癌
肾癌
Grossly:
?Most commonly at the upper pole
?Usually spherical masses
? Cut surface is colorful,yellow-
gray-white marked with areas
of hemorrhage and necrosis
Histologically:
? ―Clear cells‖ type
?,Granular cells‖ type
Intergradations
may
be
found
Classification based on
molecular origin:
1,Clear cell carcinoma
2,Papillary carcinoma
3,Chromophobe cell carcinoma
肾透明细胞癌
The most common type
?Consists of ―clear cells‖
?The tumor cells may cluster in nests,
tubers or cords
1.Clear Cell Carcinoma
2.Papillary Carcinoma
? Tumor cells line like papilla
? Obvious membrane
? Light basophilic cytoplasm
Have a comparatively
good prognosis
3.Chromophobe carcinoma
[Spread]
?1.Local invasion
?2.Metastasis：
? Hematogenous,early happened,
Unusual organs are involved,
such as mouth,larynx,eyepit,
vagina,
? Lymphatic,renal hilum,
paraaorta lymph nodes
1,Hematuria,flank pain and palpable mass
2,Fever,malaise,lose weight
3,Some tumors produce a variety of
hormone-like substance,
Renin hypertension
Hemopoietin polycythemia
Parathormone analog hypercalcemia
[Clinical course]
肾透明细胞癌
Nephroblastoma
( Wilms’ tumor)
? The third most common organ
malignant tumor in children under
the age of 10 years,and the most
common in kidneys,
? Peak incidence is 2-4 years
? Rare cases occur in adults
[Grossly]
? Usually unilateral( about 90%)
? Generally large,spherical masses
with clear boundary
? Cut surface,
?Soft; fish-flesh areas;
?Gray,hyaline cartilaginous tissue;
?Areas of hemorragic necrosis are
common.
Morphology
肾 母 细 胞 瘤
肾
母
细
胞
瘤
Three bases
? Nests and sheets of primitive blastema
? Abortive tubules and abortive glomeruli
consists of primitive epithelial cells
? Mesenchyma； Spindle cells
Histologically:
肾 母 细 胞 瘤
原
始
肾
小
管
原始肾小球
Transitional Cell Carcinoma
(TCC) of the Bladder
[Age] Peak incidence is 50-70 years
[Position] vesical triangle and
lateral wall of the bladder
The most common malignant
tumor in the urinary system
Morphology
? Range from papillary to flat,
noninvasive to invasive,and from
extremely well –differentiated
(grade Ⅰ )to highly anaplastic
aggressive (grade Ⅲ )
cancers,
膀胱癌
LM,TCCⅠ Papillary tumors with slightly
atypical appearing transitional epithelium.
TCCⅡ have irregular papillary component,
obvious atypia
TCC Ⅲ irregular nests,extremely obvious atypia,
pathologic numerous mitoses are often seen,invade
deep to muscular layer
Atypia
Hyper-
plasia Polarity Mitoses
TCC
Ⅰ Slight >7 Slightly abnormal Rare
TCC
Ⅱ Obvious >10 Abnormal Common
TCC
Ⅲ Extremely obvious Prominent Absent Prominent
[Metastasis]
? Lymphatic spread,Local lymph nodes
? Hematogenous spread,occurs later
[Clinical course ]
Painless hematuria
Class is
over
