Disease of the urinary system

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Disease of the urinary system

• Tian Dong Ping(??? ??)
• ?????????????
• 2003?5?

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Section 1 Introduction

• A. Anatomy of kidney
• Cut surface of kidney
• Cortex
• Medullary
• Renal papilla
• Calyx
• Renal pelvis

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B. Histology of kidney

• Nephrons include glomerulus and renal tubulus.
• Glomerulus Bowmans capsule and capillary tuft.

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C. Ultrastructure of glomerulus

• 1. Glomerular filtration barrier
• basement membrane (B. M)
• endothelial cell
• Visceral epithelial cell (podocyte),
  foot-process have plenty negative ion substances
  (heparan etc)

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• 2. Glomerular mesangium structure
• mesangial cell
• mesangial matrix

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D. Classification of urinary system disease

• 1. Glomerulonephritis
• 2. Pyelonephritis
• 3. Tumor of kidney
• 4. Tumor of bladder

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Section 2 Glomerulonephritis (GN)

• A. Definition
• Glomerulonephritis is a hypersensitivity
  inflammatory diease. It cause by various immune
  complex and eppear diffuse glomeruli
  proliferative inflammation in bilateral kidney

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B. Etiology and Pathogenesis

• 1. Antigen
• Endogenous antigen
• GBM, endothelial cell, mesangial cell
• Exogenous antigen
• bacteric, virus, fungus, parasit, drug ect

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2. Immune complex

• (1) In site immune complex 10
• Antibodies react directly with, intrinsic
  tissue antigen (GBM) or antigen planted planted
  (noglomerular antigen)

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• Immunofluorescent (IF) appear linear pattern or
  granular pattern .

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• (2) Circulating immune complex 90
• The antigen and antibody have not immunologic
  specificity for glomerular constituents,
  antigen-antibody complex are formed in the
  circulation and then deposit in the glomeruli. IF
  appear granular pattern.

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3. Pathogenesis
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C. Classification and pathological-clinical
character

• ?. Acute diffuse proliferative GN
• ?????????????
• (endocapillary proliferative GN,
  poststreptococcus GN)

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• 1. Pathology
• Grossly big and red kidney flea-bitten
  kidney

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1. Pathology

• LM All the glomerule are enlarge, and filled
  with nuclei (endothelia and mesangial cell),
  capillary lumen narrowed.

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EM and IF endothelial cell and mesangial cell
proliferate, in the basement membrane and under
the podocyte have hump-shaped deposite. IF appear
granular pattern
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2. Clinical-pathological correlation

• Acute nephritis syndrome
• Oiguria or anuria
• Proteinuria, cast ()
• Hematuria
• Edema
• Hypertension
• Glomerulo filtration ?

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• 3. Result 95 would be cured, 5 might turn to
  chronic GN, and few cases develop rapidly
  progressive GN.

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• ?.
• rapidly progressive GN, crescentic GN
• ??????????(?????????)
• Diffuse extracapillary proliferative GN
• 25 of this type be accompanied by acute
  nephritis and 25 of this type be accompanied by
  good pasture syndrome. 50 of this type the cause
  is unknown.

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1. Pathology

• (1) LM Epithelia of parietal layer of Bowmans
  capsule proliferates and monocytes, fibrin
  infiltrate into Bowmans capsule. Forming
  crescent (cellular crescent). Them fibrosis and
  adhesion with the tuft. (fibrous crescent). The
  Bowmans capsule cavity obstruct. The glomerulus
  develop hyalinigation rapidly progressively.

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• (2) grossly big and white kidney
• (3) EM and IF
• EM disclose subepithelia deposites in some
  cases, but in all cases show focal ruptures in
  GBM.
• IF exhibit granular immune deposites in acute
  nephritis. Linear fluorescence in goodpasture
  syndrome cases.

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2. Clinical-pathological correlation

• Rapidly progressive nephritis syndrome
• Hematuria
• Proteinuria
• Oliguria and anuria
• Rapidly progressing renal failure

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3. Result

• (1) It is very bad, the prognosis depend to the
  number of crescent
• 50 crescent prognosis well
• 50-80 crescent progress slowly
• 80-90 death
• (2) Turn to chronic sclerosing GN

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? Diffuse membranous GN ??????????(membranous
nephritis)

• Early chronic nephritis, the duration is slow
  and prognosis is relatively good

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1. Pathology

• (1) LM basement membrane diffusely thickened
  very much (platinic ring-like), but the capillary
  lumen is not obstructed usually. No cell
  proliferation.

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• (2) grossly big and white kidney.
• (3) EM There are dome and spike. Done is the
  deposit, spike is the proliferation of basement
  membrane substance so the BM becomes thickened
  and late stage BM becomes moth-eaten like.

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2. Clinical-pathological correlation

• Typical nephrotic syndrome
• High proteinuria
• High edema
• High cholesterolemia and lipidemia
• Low blood albumin

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• 3. Result
• The duration is slow. Most of cases develop
  recurrent, in late stage a number of glomerulus
  develop fibrosis, some cases may be cure.

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? Diffuse membranous proliferative GN
?????????????(mesangiocapillary GN)

• It is a chronic progressive nephritis it
  affect the mesaniun and capillary of glomerulus.
  It is more serious than membranous nephritis its
  prognosis is worse, easier to transit to atrophic
  kidney.

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1. Pathology

• (1) LM The glomerulus becomes lobulated,
  capillary wall thickened and lumen narrowed. Some
  hyaline glomeruli would be seen.

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• (2) EM Mesangial cell and mesangial matrix
  proliferate very much further more, they would
  insert into the capillary wall, the BM show
  splitting (two layer). Making the lumen seriouly
  narrow, the immune deposite can be seen elsewhere
  (mesangium and capillary wall).

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2. Clinical-pathological correlation

• The early stage proteinuria and hematuria is
  mild degree.
• The disorder affect BM nephrotic syndrome
• The late stage hypertension and renal failure.

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3. Result

• The prognosis is worse easier to transit to
  atrophic kidney, the 50 of cases develop chronic
  renal failure within 10 years.

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? . Minimal change glomerulonephritis
??????????(Lipoid nephrosis)

• 1. Pathology
• (1) Glossly big and white kidney
• (2) LM glomeruli no change at all
• tubules fatty degeneration.
• (3) EM The unique change under EM is foot
  processes fusion. No deposit at all.

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2. Clinical-pathological correlation

• Nephrotic syndrome
• (1) High proteinuria (mainly is albumin)
• (2) Hypoalbuminemia
• (3) High edema
• (4) Hyperlipidemia and hypercholesterolemia

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3. Result

• The prognosis is good 90 of cases in children
  would be cure with cortisone

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? . Diffuse sclerosing GN ???????????(Chronic
nephritis)

• This type is the final result of a lot of GN,
  its character is majority of glomeruli become
  hyaliniged, fibrosis, so renal failure, even
  uremia.

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• (2) grossly granular atrophy of kidney

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1. Pathology

• (1) LM
• Most of glomeruli are partially or completely
  scarred and some converted to hyaline masses the
  nearby tubules are atrophy and fibrosis
• Fibrosis of interstitial tissue is prominent, and
  there is an inflammatory infiltration in stroma
• Relatively normal glomeruli occur compensation
  glomeruli occur hypertrophy and tubules dilate

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2. Clinical-pathological correlation

• Chronic nephritis syndrome
• (1) Renal failure azotemia? uremia
• (2) Hypertension
• (3) Proteinurea and edema are not severe
• (4) Polyuria and noturnuria

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3. Result

• Prognosis is very bad the death cause are
• (1) uremia
• (2) Hypertensional heart disease and cerebral
  hemorrhage
• (3) Infection

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The Kidney 15

• IgA Nephropathy (Berger Disease) is the most
  common glomerular disease.
• Presence of prominent IgA deposits in the
  mesangial regions. Dx by immunocytochemical
  techniques.
• Frequent cause of recurrent gross or microscopic
  hematuria, nephrotic syndrome may be present.
• Affect children and young adults, variable
  courses.
• Associated with gluten enteropathy, liver
  disease.

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The Kidney 13

• Focal Segmental Glomerulosclerosis (FSG)
• Sclerosis of some glomeruli portions of
  capillary involved. Clinically show nephrotic
  syndrome or heavy proteinuria. Idiopathic
  responds poorly to steroids and progress to
  chronic renal failure.
• Causes associated with HIV, drug abuse,
  sickle cell disease IgA nephropathy, certain
  inherited disease and as primary disease,
  idiopathic.

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Section 3 Pyelonephritis

• A. Definition
• Pyelonephritis is a suppurative inflammation of
  renal pelvis and renal stroma, it is caused by
  pyogenic bacteritic infection directly

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B. Etiology and pathogenesis

• ?. Etiology colon bacilli (60-80)
• proteus
• staphylococci etc

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?. Infective path

• 1. Ascending infection
• Urethra?bladder ? ureter ? renal pelvis
• Organism colon bacilli women affect more easily

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• 2. Descending infection (hematogenous)
• Primary focus ? blood stream ? kidney ? cortex
  ? renal pelvis
• Organism staphylococci

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? The role of urinary tract obstruction

• gravidity uterus
• Urinary stone ? urinary tract obstruction
• prostate hyperplasia
• ? Defensive function of urinary tract?
• (IgA ?, WBC ?, clearance role of urine flow ?)
• ?bacteria grow in the urine (culture medium)

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C. Pathological type

• ?. Acute pyelonephrity
• 1. LM renal stroma and pelvis develop
  suppurative inflammation, forming abscess mainly
  .
• Ascending infection pelvis and renal stroma
  predominance
• Descending infection glomeruli and renal
  tubule around first affect

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• 2. Grossly The kidney is enlarge, surface show
  size and shape irregular abscesses, some
  abscesses are long shaped according to the
  medulla radiate streak structure, pelvis
  hyperemia and even purulent exudate covered.

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• 3. Clinical-pathological correlation
• (1) Infective symptom
• (2) Bladder irritation
• (3) pyuria, proteinuria, casts in urine,
  hematuria

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• 4. Result
• The most of cases would be cure, but when its
  treatment is uncomely, it may be recurrence and
  turn to chronic pyelonephritis.

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? Chronic pyelonephritis

• Acute pyelonephritis would transit to chronic
  the cause may be as follows
• Treatment not thorough enough
• Bacteria metamorphosis (become L- type )
• Urinary tract obstruction

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• 2. Grossly Irregular scars scattered at the
  kidney cortex become thin, pelvis and calices are
  dilated, the mucosa is coarse Large scar concave
  atrophy of the kidney

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• 1. LM
• (1) Chronic purulent inflammation, fibrosis
• (2) Renal parenchyma destruction hyalinized
  glomeruli and atrophic tubules are evident but
  some dilated tubules have big cast inside
  (thyroid tissue like )

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3. Clinical-pathological correlation

• The symptoms are not marked
• (1) Urorrhagia
• (2) Neutrophils in urine will add
• (3) Urine culture bacteria will ()
• (4) final, hypertension and renal failure

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• 4. Result
• The prognosis is poor most of cases die dead
  cause
• (1) Renal failure urinaemia
• (2) Hypertensive heart disease and hypertensive
  brain disease

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Section 4 Renal carcinoma (renal cell carcinoma,
clear cell carcinoma )

• A. Definition
• Renal carcinoma is a malignant tumor, it is
  originate from renal tubule epithelium

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B. Pathology

• ?. Grossly
• Nodular, might have a pseudo capsula, usually
  on the upper pole of the kidney yellow colored,
  hemorrhagic and necrotic

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• ?. LM
• The cancer cells are clear (lipid and glycogen
  deposition), nuclei not big, nucleus-cytoplasm
  ratio not large. Cancer cells arrange nest-like
  or gland-like. Stroma is scanty.

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C. Spread of tumor and clinical features

• ?. Hematogenic metastasis
• early stage , lung, bone, liver, adrenal
  gland, brain.
• Peculiar site nose, mouth, throat, vagina,
  eye
• Retrograde metastasis left kidney tumor ?
  left renal vein ?left spermatocord vein ?left
  epididymis

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?. Hematurine without pain

• ?. Atopic endocrine syndrome (para-tumor
  syndrome)????????????????????????????????

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D. Result

• The prognosis is poor
• No operation die within 1 year
• Operation 2 years survival 67
• 5 years survival 50
• 10 years survival 34

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Section 5 Nephroblastoma (embryonal
adenosarcoma, wilms tumor)

• A. Definition
• Nephroblastoma is a malignant tumor, it
  originate from embryonal cell (Nephroblast).
  Usually is seen in the children, very common.

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• B. Pathology
• ?. Grossly a large clear-border, nodular, grey
  color tumor arisen from the kidney. Which is
  replaced by the tumor. The pelvis and calices are
  pressured distorted.

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• ?. LM
• Two components adenocarcinoma
• fibrosarcoma
• Sometime tumor cell would form glomerulus-like
  or tubule-like structures.
• Sometime having some well differentiated
  cartilage

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C. Result

• The prognosis is more better.
• Recently record using the operative
  treatment, chemotherapy and radiothrapy, 89 of
  cases may be cure.

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Section 6 carcinoma of bladderTransitional cell
carcinoma of bladder

• A. Definition
• Transitional cell carcinoma of bladder is a
  malignant tumor. It originate from transitional
  cell of bladder. It occupy 90 of cases in
  carcinoma of bladder.

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• B. Pathology
• ?. Grossly
• Usually it is a papillary tumor with slender
  or broad pedicle, sometime it show
  cauliflower-like or polypous, sometime it is
  flat.

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• The key is to decide whether the tumor has
  invaded the underline tissue or not and how deep
  is it.

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• ?. LM
• It may be divided three grade
• 1. grade ? Low malignancy, the papilla is
  covered by orderly transitional epithelium. (510
  layer).

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• 2. Grade ? The papilla epithelium having atypia
  with evident multilayer and solid focus appear
  also.

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• 3. Grad ? high malignancy, the tumor cell show
  anaplastic and often deeply infiltrated without
  papilloma pattern.

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C. Clinical feature

• ?. Hematurine without pain
• ?. Bladder irritation
• ?. Urinary tract obstruction

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D. Result

• It is depend to the defferentiation and
  infiltration of the tumor.
• Grade ? postoperation 5 years survival 90
• Grade ?, ? recurrence 6090

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• Thanks!