Urinary System

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Chapter 10

• Urinary System

Tang Xiping
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Contents

• Glomerulonephritis
• Pyelonephritis
• Tumors of the kidney and bladder

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Questions

• How many patterns can inflammation be
  classified into?
• Which three patterns?
• What kind of inflammations
• are glomerulonephritis and
• pyelonephrits?

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structure
kidney
ureter
bladder
urethra
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• Nephron

Glomerulus
tubule
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Normal Structure of glomerulus

Vascular pole
Capillary loops
Mesangium
Renal saccule
Urinary pole
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Capi. loops
Bowmans space
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Glomerular filtering membrane
Fenestrated capillary

GBM
Podocytes
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• Function
• 1. Form and discharge urine
• Excretes the waste
• Regulates water and salt
• Maintains acid balance

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2. Excrete hormone Renin to regulate blood
pressure Erythropoietin
to generate RBC
1,25-dihydroxycholecalciferol
to absorb calcium
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Segment 1

• Glomerulonephritis (GN)

All are proliferative and most are
immunologically mediated.
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Mesangial cells

Epithelial cells
Proliferation of
Endothelial cells
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Pathogenesis
Immune Complex Nephritis in situ
Two forms
Circulating Immune Complex Nephritis
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1. Immune Complex Nephritis In Situ
1) Anti-GBM Nephritis 2) Heymann Nephritis
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• 1) Anti-GBM Nephritis
• Fixed antigens in the glomerular basement
  membrane
• Linear continuous pattern of localization by
  immunofluorescene microscopy

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2)Heymann Nephritis
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• Planted nonglomerular antigens
• Granular pattern of localization
• by immunofluorescene
• microscopy

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The glomerul is an innocent by stander?
The antigen is not of
glomerular origin.
2.Circulating Immune Complex Nephritis
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Endogenous
The origin
Exogenous
Unknown
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In the mesangium
Three sites Of Deposits
Subendothelial
Subepithelial
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3. Cell-Mediated Immune Glomerulonephritis
Caused by sentisitized T cells.
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4. Mediators of immune injury
Antibodies
Neutrophils
Complements
Macrophages
Monocytes
Platelets
Fibrin related products
Resident glomerular cells
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Basic pathologic change

• Hypercelullarity
• Thickening of GBM
• Inflammatary exudation and necrosis
• Hyaline change and sclerosis

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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
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Clinical manifestations

• Acute nephritic syndrome
• The nephrotic syndrome
• Asymptomatic hemauria or proteinuria
• Rapidly progressive nephritic syndrome
• Chronic nephritic syndrome

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Pathologic Types

1. Acute diffuse proliferative GN
2. Rapidly progressive GN
3. Membranous GN
4. Membranoproliferative GN

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• Focal segmental GN
• Minimal GN
• mesangial proliferative GN
• IgA nephropathy
• Chronic GN

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Acute Diffuse Proliferative Glomerulonephritis
(Endocapillary proliferative GN)
Location Diffuse, affecting almost all
glomeruli of two kidneys
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Pathogenesis

• Post streptococcal GN( related to a group A
  streptococcal infection)
• Typical immune complex disease
• Hypocomplementemia
• Granular deposits of IgG
• Complement on the GBM

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Morphology

• Macropically
• Kidneys are enlarged and red?
• Sometimes with petechial hemorrhages

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? ? ?
? ? ?
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LM 1. Proliferation and swelling of endothelial
and mesangial cells

• 
  

PSGN Normal
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2. Neutrophilic infiltrate
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• 3. Epithelial cell renal tubules
• Cellular swelling
• Fatty change
• Hyaline change
• Urinary cylinder in tubules

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Electron microscopy

• The immune complex arrayed often subepithelial
  humps nestled against the GBM
• Sometimes subendothreial
• or intramembranous

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EM
Immune complex
Subepithelial deposits
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Immunofluorenscence

• Granular pattern of localization on the
  capillary wall
• IgG and complement within
• the deposits

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Clinical course

• Acute nephritic syndrome
• Abrupt hematuria, proteinuria,
• cylindruria, oliguria,
• hypertension, edema.

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Prognosis

• Recovery
• Rapidly progressive glomerulonephritis
• Chronic nephritis
• lt1 renal failure, heart failure, hypertensive
  encephalopathy

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Rapidly progressive glomerulonephrits, RPGN

• ( crecentic glomerulonephritis)
• The presence of crescents in
• most of the glomeruli.

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Pathogenesis

1. Type? RPGN Anti-GBM disease, linear deposits of
   IgG and C3 on the GBM
2. Type ? RPGN Immune complex-mediated disorder
3. Type ? RPGN Pauci-immune type

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Morphology

• Macroscopically
• The kidneys are enlarged and pale.
• Often with petechial hemorrhages

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Light microscopy
The formation of crescents
The escape of abundant fibrinogen into Bowmans
space
Necrosis of capillary wall
Proliferation of parietal epithelial cells
Crescents formed
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• Early stage
• Parietal epithelial cell Monocytes
  Cellular crescents
• Fibrocytes Fibrous - cellular crescents
• Late stageFibrous tissue fibrous crescents
• The crescents obliterate Bowmans space and
  compress the glomeruli

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Electron microscope

• Distinct ruptures in the GBM in all cases,
  irregularly thickening of GBM
• Subepithelial deposits in some cases.

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Immunofluorenscence

• Linear pattern
• Granular pattern
• Lack of deposits

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Clinical course

• Rapidly progressive nephritic syndrome
• Abrupt hematuria, proteinuria,
• anuria, oliguria, anaemia,
• renal failure

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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

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Goodpasture syndrome
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Membranous Glomerulonephrits

• Basic change Diffuse thickening of the GBM
• Slowly progressive disease, most common between
  ages 30-50 years.

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Morphology

• Grossly
• Kidneys enlarged and pale.

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• LMThickening of the capillary wall

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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

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EM
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Immunofluorescence

• Typical granular deposition of immunoglobulins
  (IgG) and complement( C3) along the GBM

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Clinical course

• Nephrotic syndrome
• Heavy Proteinuria
• Hyperlipedemia
• Severe edema
• Hypoalbuminemia

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Membranoproliferative Glomerulonephritis

• Basic change
• Alterations in the basement membrane and
  mesangium
• Proliferation of glomerular
• cells

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Morphology
LM

• Proliferation of mesangial cells as well as
  infiltrating leukocytes extending into the
  peripheral capillary loops.

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• The capillary loops have lobular appearance
• The GBM is thickened , and shows a double
  contour or tramtruck apperance

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HE
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Electron microscope

• Type?Subendothelial electron-dense deposits
• Type?The lamina densa and the subendothelial
  space of th GBM are transformed into an
  irregular, ribbon-like, extremely electron-dense
  structure dense deposit disease

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Immunofluorescence

• Type ? C3 deposited in a granular pattern and
  IgG and early complement components(C1q and C4)
  are often present
• Type ? C3 is present in irregular
  granular-linear foci in the GBM and mesangium .
  IgG is usually absent ,as are C1q and C4

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Clinical course
The principle mode of presentation is the
nephrotic syndrome
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Chronic Glomerulonephritis

• (Diffuse Sclerosing Glomerulonephritis)

• Kidneys symmetrically contracted
• Surface red-brown and
• diffusely granular

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Light microscope

1. Advanced scarring of glomeruli and Bowmans
   spaces. Sometimes complete replacement and
   hylalinization.
2. Compensatory hypertrophy of remained nephrons

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• Interstitial fibrosis, lymphocytic infiltrate
• Small arteries thick-walled, with narrowed lumina

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Clinical course

• Chronic nephritic syndrome
• Diuresis, nocturia, oliguria, auria
• Hypertensoin
• Anaemia
• Azotemia renal failure

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Segment 2

• Pyelonephritis

location Interstitium , renal pelvis ,
tubules character Suppurative
imflammation age any age . Female Male
101 classification Acute and Chronic
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Through the bloodstream
Two routes
From the lower Urinary tract
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Pathogenesis
Gram-negative bacteria , especially E. coli
Acute pyelonephritis only one kind of bacteria
Chronic pyelonephritis mixed infection
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Acute pyelonephritis

• Macroscopically
• Kidneys enlarged
• Discrete, yellowish, raised abscess on the renal
  surface

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Light microscope

• Suppurative inflammation involving renal
  pelvis, interstitium and tubules.
• Abscess formation
• Tubules are filled with pus cell and
• bacteria

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Clinical course

1. Fever, chills, leucocytes ?
2. Flank pain , bladder irritation (frequency,
   dysuria, urgency)
3. Pyuria, bacteriuria, hematuria, cylinduria (white
   cell cast)

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Prognosis

• Recovery
• Improper therapy Chronic
  pyelonephritis

Complication 1)Necrosis of renal
papillae 2)Pyonephrosis
3)Perinephric abscess
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Chronic Pyelonephritis

• A chronic tubulointerstitial inflammantion
• Renal scarring

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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

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• Thyroidization (dilated tubules
• with colloid casts)
• Chronic inflammation infiltrate involving the
  calyceal mucosa
• Some glomeruli may be involved

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Clinical course

1. Dysuria, nocturia, hypertension
2. Azotemia, uraemia

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Prognosis

• Correct therapy Incomplete recovery
• Abroad lesions Hypertension, renal failure
• Unilateral serious disease
• Nephrectomy

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Class is over
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Segment 3

• Tumors of the kidney and bladder

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structure
kidney
ureter
bladder
urethra
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• Renal cell carcinoma
• Nephroblastoma
• Transitional cell carcinoma of
• the bladder

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Renal cell carcinoma

• Adenocarcinoma arising from the renal tubular
  epithelium
• Represents about 85 of all primary malignant
  tumors of the kidney
• MaleFemale 21

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• Grossly
• Most commonly at the upper pole
• Usually spherical masses
• Cut surface is colorful, yellow-
• gray-white marked with areas
• of hemorrhage and necrosis

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Histologically
Intergradations

• Clear cells type

• Granular cells type

may be found
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Classification based on molecular origin

1. Clear cell carcinoma
2. Papillary carcinoma
3. Chromophobe cell carcinoma

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1.Clear Cell Carcinoma

• The most common type
• Consists of clear cells
• The tumor cells may cluster in nests , tubers or
  cords

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2.Papillary Carcinoma

• Tumor cells line like papilla

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3.Chromophobe carcinoma

• Obvious membrane
• Light basophilic cytoplasm
• Have a comparatively
• good prognosis

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• Spread
• 1.Local invasion
• 2.Metastasis
• Hematogenous early happened.
• Unusual organs are involved, such as mouth,
  larynx, eyepit, vagina.
• Lymphaticrenal hilum,
• paraaorta lymph nodes

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Clinical course

• Hematuria ,flank pain and palpable mass
• Fever, malaise, lose weight
• Some tumors produce a variety of hormone-like
  substance
• Renin
  hypertension
• Hemopoietin
  polycythemia
• Parathormone analog hypercalcemia
  

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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

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Morphology

• 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.

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Histologically

• Three bases
• Nests and sheets of primitive blastema
• Abortive tubules and abortive glomeruli consists
  of primitive epithelial cells
• Mesenchyma Spindle cells

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Transitional Cell Carcinoma (TCC) of the Bladder
The most common malignant tumor in the
urinary system

• Age Peak incidence is 50-70 years
• Position vesical triangle and
• lateral wall of the bladder

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Morphology

• Range from papillary to flat,
• noninvasive to invasive, and from
• extremely well differentiated
• (grade ?)to highly anaplastic
  
• aggressive (grade ?)
• cancers .

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LM TCC? Papillary tumors with slightly atypical
appearing transitional epithelium.
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TCC? have irregular papillary component,
obvious atypia
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TCC ? irregular nests, extremely obvious
atypia, pathologic numerous mitoses are often
seen, invade deep to muscular layer
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Atypia Hyper-plasia Polarity Mitoses
TCC ? Slight gt7 Slightly abnormal Rare
TCC ? Obvious gt10 Abnormal Common
TCC ? Extremely obvious Prominent Absent Prominent
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• Metastasis
• Lymphatic spreadLocal lymph nodes
• Hematogenous spread occurs later
• Clinical course
• Painless hematuria

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Class is over