renal pathology blok 13

8/11/2019 Renal Pathology Blok 13

1/71

Disease of the urinary

system

Rohadi

Lab PA FK UNRAM


2/71

Kidney Anatomy:


3/71

Kidney Histology :


4/71

Kidney Histology


5/71

Kidney Histology


6/71

Classification of urinary

system disease

Congenital

Infeksi : Parenchim, Interstial Nephritis

Glomerulo Nephritis

Vascular disorder :

Hipertensive Neprosclerosis

-A.C.N.( Acut Cortical Necrosis)

-A.T.N.( Acut Tubular Necrosis )

-Infark Ginjal


7/71

SINDROME PD KELAINAN GINJAL

Neprotic Syndrome

Nepritic Syndrome

A.R.F.( Acut Renal Failure)

C.R.F ( Chronic Renal Failure )

Hidroneprosis +Hidrocalices

Calculi renalis ( Batu Ginjal )

Tumor-tumor ginjal dan kandung kemih

Benign Tumor

Malignant tumor


8/71

Preparat yang ada :

1. TCC

2. TBC Ginjal

3. Pyelonefrosis Khronis

4. PNC

5. Nerfrolitiasis

6. Pyelitis Chronic

7. Nefroblastoma

8. Glomerulonefritis

Kronis

9. Renal Cell Ca

10. Squamous Cell CaGinjal


9/71

TBC Ginjal

Renal tuberculosis. Photograph of a cut gross specimen shows multiple,

predominantly peripheral, white tuberculous granulomas throughout the kidney.


10/71

TBC Ginjal


11/71

Normal

Proliferative

Post strepto


12/71


13/71

Chronic glomerulonephritis

Chronic glomerulonephritisrepresents the end-stage of all

glomerulonephritis with unfavorable evolution. This general (glomerular,vascular and interstitial) affection constitutes the so-called "end stage

kidney". In most cases, it is associated with systemic hypertension.

a kidney with chronic glomerulonephritis. The cortex has largely

turned to scar tissue and there is a poor demarcation between

cortex and medulla due to the glomerular scarring.

h l l h


14/71

Chronic glomerulonephritisThe majority of the glomeruli are affected.

Depending on the stage of the disease,

they may present different degrees of

hyalinization (hyalinosclerosis - totalreplacement of glomeruli and Bowmann's

space with hyaline). The hyaline is an

amorphous material, pink, homogenous,

resulted from combination of plasma

proteins, increased mesangial matrix and

collagen. Totally hyalinised glomeruli are

atrophic (smaller), lacking capillaries,

hence these glomeruli are non-functional.

Few glomeruli may still present changes

which permit to discern the etiology of

chronic glomerulonephritis. Obstruction ofblood flow will produce secondary tubular

atrophy, interstitial fibrosis and thickening

of the arterial wall by hyaline deposits. In

the interstitium is present an abundant

inflammatory infiltrate (mostly with

lymphocytes).


15/71



16/71


Functional nephrons have dilated tubules, often with hyaline casts in the lumens.


17/71

Pyelonephrosis

An absolute term for any disease of the pelvis

of the kidney. ... Origin: pyelo-+ G. Nephros,

kidney, + -osis,


18/71

Acute pyelonephritis

route of invasion :

via blood stream

ascending route

obstructive

non-obstructive

role of vesicoureteral reflux and infected urine


19/71

PYELONEPHRITIS ACUTA

Makroskopis :

-.Uni/Bilateral

-. Ginjal>> Kapsul meregang

- Abses kecil sub kaps,Pelvis hyperemis

granuler.

-URINE : PURULENT

Mikroskopis :

-Gambaran Abses

Akibat: Resolusi, Chronic Pyel., Supp, Bisa +


20/71

Septicemia-

Microabscess


21/71

Septicemia-Microabscess


22/71


23/71


24/71


25/71


26/71

CHRONIC PYELONEPHRITIS

Makroskopis : Ginjal Mengecil

Kapsul melekat, menebal( parut) Cortex tipis

Batas dg medulla kabur,warna pucat

Medulla mengkerut

Pelvis menebal fibrotik,pucat Calyces melebar

Vasculer prominent


27/71

CHRONIC PYELONEPHRITIS

Mikroskopis :

Parenchym : Kelompok jar.parut.

Tubulus : Delatasi,epit.atrofi : berisi bahan albominus (koloid/ Tiroidisasi)

Asal : Dr.proses inf ringan,lama,berkelanj.

-Pyelo.Acut Berulang


28/71

PNC

You can see the stones, dark red and rough. They have plugged the renal

collecting system and dilated the calyces. Stasis of urine and the presence of the

inert stones themselves both promote infection. This in turn can make the stones

grow larger.


29/71


30/71


31/71


32/71

Microscopic View of PNC

1. scarring and shrinking of the renal tubules, with the glomerulus spared.In contrast to rapidly progressive glomerulonephritis, the scar is outside

Bowman's capsule.

2. a group of tubules filled with cast protein and distended from scar

contraction. The unwary may mistake this for thyroid.


33/71

Urolithiasis :


34/71

Urolithiasis:


35/71

NEPHROLITHIASIS


36/71

Staghorn Calculus:


37/71

NEPHROLITHIASIS

Top left: Retention of calcium oxalate crystals in the renal tubules after kidney

transplantation. Top right: Close-up image of calcium oxalate crystals plugging the renal

tubules of a primary hyperoxaluria patient with end-stage renal failure. Obstruction of the

renal tubules leads to tubular necrosis and loss of the total nephron mass. In preterm

infants, tubular nephrocalcinosis may lead to reduced renal function in adulthood, while in

renal transplant patients it may have a negative impact on long-term graft survival.


38/71

Hidronefrosis


39/71

Urolithiasis with hydronephrosis:


40/71

Hidronefrosis

Obstructive uropathy; form a continuousspectrum from minor changes of blunting

of the renal papillae to severe from where

kidney converted into a multiseptate sac

with paper-thin walls.


41/71

Hidronefrosis

1. Thinning renal parenchyma with residual large renal vessels in the hilum;

note dilated renal pelvis with flattened epithelia.

2. Sclerosis of glomeruli with atrophic tubules; note renal pelvis with flattened

epithelia.


42/71

TUMOR GINJAL

Benigna : Adenoma

Hamartoma

Haemangioma

Lipoma,Angiomio lipoma,Fibro

ma, liomyoma.

Maligna : Adeno Ca, Grawits tu, Willm Tu,Sarcoma


43/71

Renal carcinoma(renal cell carcinoma, clear cell carcinoma,

grawit tumor )

Definition:

Renal carcinoma is a malignant tumor, it

is originate from renal tubule

epithelium . 80

90 %. Age : 60

70 th.

Risk Factor : Smoking


44/71

RCC

This renal cell

carcinoma is very large,

as indicated by the 15

cm ruler. A portion ofnormal kidney

protrudes at the lower

center. This patient was

a physician himself andjust didn't have any

early symptoms.


45/71

RCC (GRAWITS TUMOR)

Morfologi : Makros

Tumor besar 3-15 cm

Pd irisan : Kuningabu2 dg area kis

tik & perdrhn prominent

Ada satelit nodul

Bisa meluas : Ke Collect Tub---Calyces-------Pelvis--- Ureter


46/71

Pathology

Grossly :

Nodular, might have a pseudo

capsula, usually on the upperpole of the kidney; yellowcolored, hemorrhagic andnecrotic


47/71

Slide 21.72


48/71


49/71

Microscopic View :The cancer cells are clear (lipid and

glycogen deposition), nuclei notbig, nucleus-cytoplasm ratio not

large. Cancer cells arrange nest-

like or gland-like. Stroma is scanty.


50/71


51/71

Slide 21.73

Renal Cell Carcinoma


52/71

Renal Cell Carcinoma:

Incidence:

Etiology:

Clinical

Features:

Lab:

Path:

Clinical

Course:

Cells of proximal convoluted tubule. Risk

factors are smoking, obesity, analgesic

abuse.

Hematuria*, flank pain, palpable mass.

Frequently metastasize (lungs, bone, skin,

liver, brain).Gross or microscopic hematuria.

Specific Dx by radiographic techniques.

5-yr. survival 40%. Poor prognosis with

metastases.

Gross: Large yellow mass with hemorrhage

and necrosis. Invade renal vein.

Micro: Usually clear or granular cells with

little anaplasia. Other histologic variants

(great mimicker).

5th

and 6th

decades, most commonprimary renal malignancy.

Treatment: Chemotherapy, surgery, immunotherapy.

Synonyms: Hypernephroma, clear cell carcinoma.


53/71

Squamous Cell Carcinoma Ginjal


54/71

Squamous Cell Carcinoma Ginjal

The tumor is moderately differentiated with

formation of abundant keratin pearls


55/71

Nephroblastoma(embryonal adenosarcoma, wilmstumor)

Nephroblastoma is a malignant

tumor, it originate fromembryonal cell (Nephroblast).

Usually is seen in the children,

very common.


56/71

WILMS TUMOR("nephroblastoma"): One of thecommonest pediatric solidtumors (peak age 1-4 years).Wilms tumor microscopicallyresembles the primitive

nephrogenic zone of the fetalkidney, with primitiveglomeruloid structures and acellular stroma. Wilms tumor isassociated with mutationsinvolving the WT1 tumorsuppressor gene on chromosome

11. This neoplasm is verytreatable with an excellentprognosis and >80% cure rateoverall.


57/71

WILMS TUMOR

Makroskopis :

Tumor berukuran bbrp Cmsangat

besar

Warna putih abu2

Homogen dlm kapsel ginjal

Tampak area nekrosis & perdrhn


58/71

WILMS TUMOR

Mikroskopis :

1. Jaringan ikat

2. Blastema

3. Komp.Epit.yg dpt membent.strt.Tub,

Glomerulus ( Abortive Glom. )

Salah satu komponen bisa dominant


59/71

Microscopic View :

Two components:adenocarcinoma

fibrosarcoma

Sometime tumor cell would formglomerulus-like or tubule-like structures.

Sometime having some well differentiated

cartilage


60/71

WILM TUMOR

Wil T


61/71

Wilms Tumor

Incidence:

Etiology:

Clinical

Features:

Lab:

Path:

Clinical

Course:

Embryonic renal tissue (metanephric

blastema). Genetic abnormalities.

Palpable abdominal mass. Abdominal

pain, fever, anorexia, nausea/vomiting.

Hematuria.

No specific clinical laboratory findings.Diagnosis by radiographic techniques.

5-yr. Survival 80%. Metastases to lung,

liver, bone, brain.

Gross: Solitary/multiple cystic mass,

sharply delineated. Soft, bulging, gray-

white with focal hemorrhage and necrosis.

Micro: Triphasic mesenchymal stroma,

tubules, and solid areas (blastema).

Primitive glomeruli, skeletal muscle,cartilage, bone, etc. (embryonic tissues)

Most common renal tumor of

childhood. Peak age - 2.5 - 3.5 years.

Treatment: Prompt resection with chemotherapy

radiotherapy.

Synonyms: Nephroblastoma.


62/71

Carcinoma of Bladder

Transitional cell carcinoma of bladder

Definition

Transitional cell carcinoma of

bladder is a malignant tumor. It

originate from transitional cell ofbladder. It occupy 90% of cases in

carcinoma of bladder.


63/71

Pathology

. Grossly:

Usually it is a papillary tumor with

slender or broad pedicle,

sometime it show cauliflower-likeor polypous, sometime it is flat.


64/71


65/71

TCC Bladder


66/71

TCC Bladder

These tumors showmore architectural

disorder and nuclear

atypia than Grade 1

tumors. The nuclear

size, shape, polarity,

and chromatin show

greater variability.Mitoses are still

infrequent.


67/71

TCC Bladder

Another look at grade 1 papillaryurothelial carcinoma. These

patients are at risk of developing

recurrent tumors which may be

of higher grade. This entity is

considered synonymous withpapillary urothelial neoplasm of

low malignant potentialin the

1998 WHO/ISUP Classification of

papillary urothelial neoplasms.


68/71


69/71


70/71


71/71

renal pathology blok 13

Documents