Anda di halaman 1dari 3

WorkshoP nr L9 - Renal PathologY I

MICROSCOPY-MI

Topic

l.

Acute postinfectious diffuse GN (MO' ME)

2.

Progressive raPid GN (MO)

3.

Minimallesion GN (ME)

4.

Idiopathic membranous GP (ME)

5.

Diabetic GS (PAS, MO)

6.

Chronic GN (MO)

MACROSCOPY-MA

Glomerular nePhroPaties

1. Lipoid nephrosis

2. Chronic GN

II. Obstructive uroPathY

l.

Urolithiasis

2.

Hydronephrosis

III. Malformations

l.

Horse Shoe kidney

2.

Polycystic kidneY

3.

Kidney with double pelvis and double ureter

Renal diseases

.

.

.

MICROSCOPY-MI

Glomerular nephropathies - GN

Tubulo-interstitial nephropathies Q'ITI)

Vascular NPs-vascular kidney damages in HTA

Glomerular nephropathies - GN

1. Acute postinfectious diffuse proliferative glomerulonefritis

.

.

immune complication

with diffuse involvement of glomeruli that occurs at2-4

weeks after an

ME - large electron-dense nodular deposits of immune complexes disposed on the

infection with B haemolytic streptococcus group A

external surface of GBM
.MO

. diffuse glomerular lesion: all glomeruli are affected simultaneously,

bilaterallY

'g1'meril*i':i:il3lffr:f1";h+l jllifffi i].u,i,.,u.u,i.n.r

capillary lumen

. tenal tubules are normal

2. Rapid progressive glomerulonefritis (RPG)

^

.

.

.upid atrd ptogtessive loss of renal function

Mb - profiferation of parietal epithelial

obstruction of Bowman space and compressing of the glomerular capillaries

in several months and death

with

cells of Bowman capsule )

MO-optic microscoPY

ME-electronic microscoPY

3. Minimal change GN (lipoid nephrosis)

EM .

.

primary lesion is on glomerular )

fusion of extracapilary epithelial cell processes

epithelial cells come into direct contact with the GBM, which becomes permeable

with loss of lipoproteins, which are reabsorbed at the level of renal tubules

MO

.

.

glomenrli are normal

proximal tubular epithelial cells are loaded with lipids )

old term of lipoid

nephrosis reflects the presence of numerous fat drops into renal tubules

4. Idiopathic membranous GP (ME)

EM

.

early, immune complex deposits on the external surface of GBM with GBM expansion between these deposits looking as radiary spikes (aspect of wheel)

.

late, the spikes fuse and include immune deposits resulting alacy appearance

MO - thickening of basement membrane of golmerular cappilaries

5. Diabetic GS (PAS--MO)

MO-3 types of glomerular lesions

a. GBM thickening is the

(+) deposits

most early form of diabetic microangiopathy : PAS

b. diffuse GS (Sdr. Bell) consists of diffuse deposits of PAS (+') material into

glomerular mesangium

c. nodular

GS (Kimmelstiel-Wilson sdr) consists of nodular deposits of PAS (+)

material into glomerular mesangium Evolution-deposits increase with obliteration of capillary lumen and development of CRF

6. Chronic GN (MO)

 

.

end stage of glomerular nefropathies; the main cause of chronic renal failure

MI

 

.

Glomeruli are hyalinized and corresponding tubules are replaced by connective

 

tissue

 

o

I reduced number of glomeruli and tubules are hypertrophied, (increased in

 

volum but with a normal function) giving the appearance of cortical microgranulararitY

 

.

There is a marked interstitial fibrosis associated with chronic inflammation

MACROSCOPY-MI

I. Glomerular nephropaties

1. Minimal change

. kidneys u.i

disease (lipoid nephrosis)

itt.t"uted of volume, the renal cortex being pale-yellow (by

accumulation of lipids in the tubular epithelium) and with smooth external surface

2. Chronic GN

.

.

both kidneys are atrophied, pales with an adherent capsule and fine granular

external surface

On the cut section, the cortex is atrophied with hilar adipose tissue hyperplasia

II. Obstructive uroPathY

-

-

-

-

Urolithiasis

^.

renal

disease characterized by abnormal precipitation of urinary salts with

formation of solitary or multiple, uni or bilateral calculi (calcium oxalate, calcium

phosphate, etc )

Locations (2)

pielo - caliceal system

o

o

bladder

small and multiple calculi through mobilization produce lumbar pain

large calculi cause obstruction and urinary stasis (hidronephrosis and

secondary infections)

.

.

.

o

o

^.

calculi coming from ureter

local calculi secondary formed by urethral obstruction

HydronePhrosis

renal

pelvis dilation caused by chronic obstruction of the urinary tract of different

causes

Causes: nodular prostate hyperplasia, calculi, malignant tumors

Macroscopy (2 evolutive forms):

"' j"'n*#:g,l*ru;ff i;lfl ffJli:#1tri?$war*hinning

seclndlrulJlJ:?r'"I,li"",itr,n. renal pelvis, with verv thin wau

' irreversible atrophy and fibrosis of renal parenchyma

Ill.Malformations

.

.

.

. Horse Shoe kidneY

the fusion by connective tissue of the 2 kidneys at the inferior or superior poles

the ureters are located on the front aspect of the kidneys

the renal function is not affected

. Polycystic kidneY

- the presence of cysts in the kidney - 2 types: adult and infantil tYPes

Adult type

.

-enlarged and irregular kidneys (4 kg), composed of various sized cysts, (5-6 cm)

containing a serous or bloody fluid, separated from normal renal parenchyma

Infantil type

. -kidneys are enlarged and have a preserved shape; they are spongious on the cut

surface due to the presence of cystic fusiforme dilatation that extend radiary to the

cortex and medulla.

. Kidney

with double pelvis and double ureter

the 2 ureters

can fuse to a point above the bladder junction or they may have

entire separate courses with different bladder entrances