Tractus urinarius

Dr.Resmi Kartini

KERUSAKAN GLOMERULUS

1.Out put urin menurun

2.Proteinuria
3.Hematuria

Swelling of endothel

loss of
Blood flow
epithelium

endotel

Urin
hematuria

inflamation
altering

focal

permeability
of layer

proteinuria

Kerusakan tubulus
1.Loss of mechanisms controlling balance
of electrolytes,water
2.upset in acid base balance
3. Loss of substances in urine normally
completely or almost completely
reabsorbed glucose,potasium,amino acids
4.Proteinuria due to damage to associated
capillary

Simple diag.test pada kerusakkan ginjal

1.

2.

Urine : protein,red ceels,hb,pmn

Urinary casts :
* protein ( hialin / colloid )
* Red cells
* Epithelial casts - desquamasi epit.tub
* Granular sel tub necrosis
* Kristal

B.Kimia darah

Urea ( 2.5 7.0 m mole/ lt )

Creatinin ( 50 100 mole / lt )
C02 ( 22- 28 m mole / lt )
Clearance test

Manifestasi klinik pada ginjal

Azotemia BUN
( blood urea nitrogen )
Creatinin
GFR
PU
Renal
Disorder

Pre renal

( perdarahan,shock,Vol deplet
ion ,congestive heart failure )

- kerusakkan parenkhim ginjal (-)

Post renal obstruksi

gejala klinik
Biokimia aqbnormal

Uremia

Mayor Renal syndrome

1.Sindr.nefritik akut : sindr.glomerulus

hematuria.proteinuria,hipertensi
pd glom.is post strept
2.Sindr nefrotik: proteinuria berat(> 3,5 gr/hr)
hipo albuminemia
edema berat
hiperlipidemia / lipiduria
3.Hematuria / proteinuria asimtomatik
4. R F A - oliguria anuria -- azotemia

5. RFC : uremia
5.RFC : uremia
chronic renal dis
6. Renal tubuler defect : poliuria
Nokturia
Elektrolyt disorders
(metab acidosis )
7. Urinary tract infection : bakteriuria,pyuria
8.Nefrolitiasis

Kelainan kongenital

1. AGENESIS
2.HIPOPLASIA
3.ECTOPIC KIDNEYS
4.HORSE SHOE KIDNEYS

Cystic Dis
* penting ok :
1. Mrpkan problem diagnostik : Klinisi , radiologis
,patologist
2.Polikistik adult RFC
3.Confuse dg tumor malignant

Klasifikasi :
1.Cystic renal dysplasia
2.Polycystic kidney dis
* autosomal dominant ( adult )
* recessive( childhood )
3. Medullary cystic dis : * Med Sponge kidney
* Nefronoptisis uremic med.cyst
4. Acquired ( dialysis associated ) cystic dis
5. Localizet (simple ) renal cyst
6. Kista pd malformasi herediter ( tuberous sklerosis)
7. Glomerulo cystic dis.
8. Extraparenkhimal renal cyst

Patogenesis
Genetik

Acquire
Defect

Altered epithelial cell differentiation

Abnormal
EGM matrik

Altered
cell growth

Cyst

Fluid
secretion

Cystic renal dysplasia

Diff metanefrik abnormal
Khas : Struktur ginjal abnormal persisten
- Tl rawan, mesenkhim undiff
dukt kel imature tbtk lobus abn
* Py sporadik
Kbnyk kss ~ obstruksi ureteropelvik,agenesis ureter
atresi,anomali sal kemih distal
Morfologi : Ginjal besar, irreguler, multikistik
dilapisi ep flattened
Fungsi ginjal lain : N

Autosomal dominant ( adult ) polycystic kidney dis

1 / 1000 org
10 % pd kasus transplantasi ginjal & dialisis khr
Morfol : - bilateral
- ginjal > 4 kg, 3-4 cm
- dari tubulus nepron dilap ep macam 2
Klinik : Asimptomatik insuf renal
Nyeri pdrh,kista dil progresif
kolik ekkrei bekuan darah

py ginjal khr prog

40 % ~ polikistik hati, jrg pd limpa, pancr, paru
10 -30 % aneurisma berry
: Azotemia spi uremia
RF ( 1/3 )
hipertensi (py jant, hemorrag, ruptur aneurisma berry )
unrelated cause

Autosomal recessive ( child hood ) poly cystic kidney dis:

Perinatal

Neonatal
Infatil
Juvenil
Young infant -- R.F
Morf : Ginjal .>> Permuk licin
Cortek,medula : multiple kista ~ Sponge Like
Mikros : Dukt collecting dilatasi - Sakuler / silendris
Dilap ep kuboid
Kbyk kasus kista liver ( dilapisi Multiple Epithelium line
cycts + prol d. bil Portae )

 survive infancy ( infatil & juv ) berkemb hepatik

fibrosis

- Cong Hep fibrosis : Fibrosis periportal

proli dukt.bil well
diff
older children hipert portal ,splenomegali
KISTA MEDULA :
1. Medullary sponge kidney : dilat kistik multiple
dukt collect pd med.
Klinik : Dukt. Dil.hematuria.inf. Batu
Morfol : Kista kecil 2 dilap ep kuboid /
transtitional

2. Nephronophthisis uremic medullary cystic

dis (umcd ) complek

Dimulai pada masa anak , progresif

Khas :
kista multiple
insuf renal
atropi tubuler
--> hereditary
fibrosis interts
tubulo interst
nephitis

1.Sporadic. Non familial ( 2o % )

2. familial juvenil nephronophthisis (50% )

3. Renal retinal dysplasia ( 15 % ) ~ retinis pigment

Klinik : Poliuria , polidipsia

Sodium lossing , tubuler acidosis
5- 10 th RF
Mikros : Kista dilat epitel kuboid. Dikelilingi jar
fibrosis & inflamasi

GLOMERULAR DISEASES
Mrp masalah pd nefrologi ok GNC pybb RF
* Primary glomerulopathies
Acut diffuse Prol G N
Post Strep
Non post Strep

Rapidly Prog. ( crescentic ) G.N

Membr. Glomerulopathy
Lipoid neprosis ( minimal change dis )

Focal segmental glom sclerosis

Membrano prol.gn
IgA Nephropathy,focal prol .g.n; GNC

*Systemic dis : SLE,DM,Amiloidosis,Good Pasture

syndr,Wageners granulomatosis,Henoch schohlein

purpura.Bact.Endocarditis.

Hereditary Disorders

ALPORTS SYNDR
Fabro Syndr

KLINIK :

Glomerular Syndr
* Acute nephritic syndr
Hematuri
Azotemia
Proteinuria
oligouria
Edem
Hipertensi

Rapidly prog G.N

* Nefritis akut
*Proteinuria
* R.F.A

R.F.K

Azotemia --- Uremia prog

* Nephrotic Synd :
Proteinuria ( > 3,5 gr )
Hipo albuminemia
Hiper lipidemia
Lipiduria

*ASYMPTOMATIC HEMATURIA / PROTEINURIA

HEMATURIA GLOMERULER
SUBNEPHROTIK PROT URIA
HISTOLOGIC ALTERATIONS
1.Hipersel Glom :
a. Prol sel mesangeal,endotel, atau sel ep
parietal. b. Infiltrasi lekosit
2. Penebalan membr. Basalis

a. Penebalan M. Bas ( D.M )

b.Deposit material amorf ( Protein ) pd

endotel/ epitel

3. Hialinisasi dan sklerosis

( Difus, global, Fokal, segmental ,

mesangeal

Acute Post Strept ( prol ) G.N

Strep hemol beta

tipe A Ag A b glom
complek

compl
(faring, kulit )

* cytoplasmic AG
( endostreptosin )
* cationik AG
*Proteinase ( strep
Erythrogenic toxic )

Planted Ag

circulating
imun

Morfol : A. Glom enlarged, hipersel, blood less relatif

hipersel 1.

prol sel endotel,mesangium

2. infiltr sel leukosit,neutropil

monosit

Sel endotel bengkak. prol

Infiltr sel leukosit
obliterasi

lumen kapiler

B. Deposit fibrin
C. Edem intersti
D. Tubulus --- casts red cell
degenerasi

Klinik :
glom capillary obstr

damage glom endothel

reduce blood flow

tub ep damage

Stimulation
of juxta

diminised
filtration

glom App

focal increase escape of

in permeabilitas red cell

fluid

retention
oliguria

Rise in blood
Pressure

rised
oedema
blood urea

unselektif
protein urea

hematuria

Casts
epithelial
protein
red cells
*malaise,nausea.edem peri orbital --------- 1- 2 mg post infeksi

PERJALANAN PENYAKIT
ACUTE DIFFUSE ( PROL ) G.N

CARDIAC FAILURE
OR UREMIA

MILD PROTEIN PERSISTING

PERSISTING FOR PROTEINURIA
MONT OR TWO

RAPIDLY

PROG. G.N
AND HEMATURIA

chronic nephritis

DEATH IN ACUTE

RECOVERY

Death years later

Rapidly Prog GN
Khas :

Akumulasi sel pd rongga bowman crescent

Klassif & patogenesis
1.Post inf ( post strept ) RPGN
2.GN Py sistemik ------ SLE,Good pastures Syndr
Vasculitis ( poli artritis nodosa )
Wegener granulomatosis
Henoch Scholein Purpura

Klinik : ~ APGN --- lebih berat

Morfol : Ginjal > >, pucat,hemor.petechiae
Glom : nekrosis focal,prol mesangeal,prol endotel focal/difu
prol endotel fokal / difus
MIKROS : Ep crescent - prol sel parietal
migrasi monosit,makrofag
fibrin
Perjln Py ~
penyebab . . Hipertensi,uremia super impuse inf
perikarditis fibrinosa, Anemia

Nephrotic Syndr.
Cause :

1.Primary glomerular dis

* Membr. GN
* Lipoid nephrosis
Focal seg. GN
Membr.Prol.GN
Other prol GN ( Focal , pure mesangeal

Ig A nephropathy )
2. Py Sistemik
* DM ,Amyloidosis, SLE
* Drugs ( penisilin, STREET HEROIN )
* INf ( malaria ,sipilis , hep B, AIDS )
* Malignancy
* Miscellaneus ( alergy, nefritis herediter )
Proteinuria >= 3.5 gr
Hipo albuminemia, Edem , Hiperlipidemia

Membrano GN / membranous nephropathy

Mrpk penyebab terbnyk pada adult
Khas ; deposit imunoglob. Containing , electron. Dence
sepanjang
epit. ( sub epitel ) membr. Basalis.
Penebalan difus dd kap
Dpt ~ sebagai Mekanisme sekunder spt :
-T. Ep maligna ( dr paru,kolon . Melanoma )
- S.L.E
- expore tu inorganic salt ( gold . Mercuri )
- drug ( penisilamine , captopril )
- infeksi ( hep.B kronic, sifilis , schistosomiasis,malaria )
- Metab disorders ( DM ,Tiroiditis )
85 % kasus idiopatik

ETIOLOGI , PATOGENESIS

DEPOSIT Ig sub epitel -- chronic Ag Ab mediated dis

Morfol : Glom : uniform , penebalan dd kap difus
deposit ireg dence diantara membr basalis
sel epit
lost foot prosessus
- pros berlanjut glom sklerosis hialinisasi ---hi
pertensi
mesangium sklerosis
Tub --- droplet hialin
Respon kortico steroid (+)
10 %
10 % R.F ( 10 thn ); , 40 % renal insuf

Minimal change Dis / lipoid nephrosis :

Terut menyebbkan N.S. pd anak ( 2-6 th )
Khas : Glom. Foot processes menghilang difus
Etiologi 1. Post infeksi resp / imunisasi
2. Respon thdp kortico steroid & terapi imunosupre
si
3. ~ Py atopik ( eczema , rinitis )
4. Minimal change ~ atopi ( genetik )
5. pd py hodgkin
6. Post transplantasi
Morfol : Glom . N. -- Foot processes fusi
Tub prox Lipid
Respon kortiko steroid ( + )

Focal segmental glomerulo sklerosis

KHAS :Sklerosis bebrapa glom , mengenai sebagian kap
Tdd : 1 idiopathic FSG
2.FSG super imposed on another primary glom lesion
( Ig Nephropathy )
3. FSG loos of renal mass ( renal ablation FSG )
dgn py ginjal stad lanjut ( renal nepropathy , analgetik abuse
nephropathy, agenesis ginjal unilat
4. Secondary FSG ( heroin . Inf HIV )
80 % - NS tetapi beda dgn yg disebabkan minimal change GN - 1.
Hematuria , GFR , Hipertensi
2.Prot. Uria non selektif
3.Respon kortico st buruk
4. Progresif - GNC ; 50% end stage ( 10 th )
5. Deposit Ig.

Morfol
Mengenai sebagian glom
Pd segmen sklerotik , membr bas kolaps
matrix mesangeal , hialinosis
PD : tebal ( hialin )
Glom sklerosis atropi tubuler- fibrosis interst
Patogenenesis : Hipert glom , kap hipert
Perub sel epit dipus - deg dan kerusakan fokal sel epit visera -
khas med - FSG
Deposit prot
fibrin
reaksi sel mesangeal

Fokus 2 permeabilitas

- hialinosis
sklerosis

Perjalanan penyakit

Idiopathic FSG ----Remisi spontan

Anak prog > baik dari adult
20% malignant fokal sclerosis -
prot uria masif -- RF kronik ( 2
tahun)
25-50% rekuren pada alograf
HIV associated nephropathy 5 10 %

Membrano prol GN
Khas : lesi pada membrana basalis
Prol sel glom
> mesangeal - masangio capillary
Primer MPGN - idiopatik
Sekunder MPGN -- sistemik disorder
Secara Mikros elektron : dibagi tipe I & II
Morfol :
Glom : Bsr , Hipersel- Prol sel mesangium
: Lobular Appearance
GBM : Tebal tu pd kapiler loop membr Basal splitting
- inklusi sel pros mesang ke kap loop perifer
- : mesangeal interposition
TIPE I : 2/3 Kss
Deposit elektron dense sub epitel ; Ig G ( + )
II : Deposit dence material posisi tdk dike -- dsbt DENCE
DEPOSIT DIS
Ig G ( - )

IgA nephropathy ( BergerS Dis )

Khas : Deposit IgA pd mesangium
Plg banyak menyebabkan hematuria rekuren
Frek
Morfol : FPGN
Diffuse mesangeal prol -- sklerosis fokal
Deposit Ig A mesangium
Perjalanan peny
Anak
inf : resp
mukosa git -- 1-2 hr
urin tract
Dewasa

IgA nephropathy ( BergerS Dis )

Klinik : Py heterogenous
Biasa benign- slowly progresif
50% RF ( 20 thn )
Terut : Prot urin brt
Hipert
ditemukan
sklerosis vasc

-- Progresif

Fokal prol dan necrotizing GN

Fokal GN : Prol glom tbts segmen glom dan bg glom

Nekr .Focal
Deposit fibrin
Fokal GN :
<---1. Manifest dini ( RGN py sist : SLE , PAN , Henoc
Schonlein pur, Good Pasture synd , Subacut
bact .endoc, Wegener S Granulomatosis
2. IgA
3. Primary idiopathic focal GN

CHRONIC GN

End state GN
Post strep GN
1-2%
RPGN
40%
MGN
50%
F.G sklerosis
50-80%
MPGN
50%
IgA
30-50%
others

CGN

Morfol :
Ginjal kontraksi simetris , granular difus
Korteks tipis , lemak peripelvic
Early : glom etiol
obliterasi hialin
prot plasma trapped , matrik
mesangeal
kolagen
arteriosklerosis
tub atropi, intersti fibrosis
- dialysis changes

- disertai CRF
uremic pericarditis
uremic Gastroenteropathy
Hiperparatiroid ---- Nefrocalcinosis
Uremic pneumonitis

__

Lesi glom akibat py sistemik

SLE
klinik : hematuria , nefritis akut
NS , CRF , Hipertensi
HIST: Mesangeal lupus nephritis
Focal GN
Diffuse Prol GN
Diffuse Membr GN

Henoch Schonlein Purpura

Tdr : lesi kulit khas : daerah extensor lengan ,kaki
, bokong ( Hemorr necrotizing vasculitis )
manifes abdomen : nyeri , V. intestinal bleeding
Arthralgia non migratory , abn ginjal
hematuria,proturia
NS, rapidly prog GN - RF
atopi post inf resp
Morfol : Prol. mesang. Fokal / difus, crescentic GN
Deposit Ig A

Endokarditis bakterialis
- immune complex GN
hematuria, prot. Uri
fokal / segmental necrotizing GN
diffus prol GN, RPGN
DIABETIC GLOMERULO SCLEROSIS
cause 30 % end stage py ginjal
20 % ---- < 40 th

Klinik :

Non nephrotic prot uri

NS,CRF,Arterioler Sclerosis, Pielo nefritis,
Necrosis papiler, Lesi tubulerp
- Nefropati Diabetik
50 % insulin dependent
Insulin independent ( tipe II )
Nefrotik
12 -22 thn - CRF 4-5 th

MORFOL :
1.Penebalan Membr. Basalis & P..
2. Glom. Sklerosis difus -
3.Glom Sklerosis Noduler intercapillary Glom SKLe.
Kimmelstiel Wilson Dis.
Glom
Hialin - Ginjal Ischemia
Arteriol
Atropi Tub
Fibrosis interst
Kontraksi

Perjalan Py :

GFR -- Micro albuminuria 20 -200

gr / menit
Prot. Uri GFR PROG.Loss RF ( 5 TH )
Hipert -- Prot uri
insuf renal

NEFRITIS HEREDITER

Alport S Synd : Nefritis

tuli (saraf )

ggn mata ( dislokasi

lensa ,katarak post, distropi kornea

berat
Hematuria, NS,
Timbul pd usia 5-20 th RF 20 th 50 th
Morf:
Glom prol Segmental & sklerosis Matrik mesangial
Foam cells - glom sklerosis, pd sempit , tub atropi
fibrosis interst

PENYAKIT TUBULUS dan interstitium

1. Ischemik / toxic tubuler injury

- ATN dan RFA
2. Inflamasi tub dan interstitium -
Nefritis tubulointersti

ATN

Khas : destruksi ep tubulus

fg ginjal akut
- RFA ( 24 jam - urin , 400 cc

----------

1. Organic vascular obstruktion

- Pd intra renal difus ( Poli artritis N,
Hipert malignant,Hemolytic uremic syndr)
2. Severe Glom. Dis ( RPGN )
3. Acute Tubulo intersti. Nephritis
( Hipersensitif drug )

4. Massive infection ( Pielonef )

Nekr.Papil
5. DIC ( pd ginjal )
6.Urinary obstruction ( Hipertr Prostat ;
Blood clot - Post renal ARF )
7. ATN

Patogenesis
Ischemic

ATN - KRSK tubulus

injury

Nefrotoxic
Ep tubulus sensitif thdp anoxia, toxin
Faktor predisposisi
1. Gg sensorik - reabsorbsi tub
2. Sist Transport ion dan organi acids
3.Kesanggupan - konsentrasi efektif

Sel epitel : Struktur }

} terganggu -- loss of polarity

Fungsi }

Sekali terjadi injuri tub - ARF progresif

1.Kerusakan tubulus vasokonstruksi
arteriol preglom GFR
2.Kerusakan tubulus oliguria tubulus
debris blok uriner flow, intratubulus
GFR
3.Cairan dari tubulus rusak jaringan
intersti tekanan intersti tubulus kollaps
4.Efek langsung toxin pada ultra filtration
glomerulus

MORFOLOGI
ATN Ischemic khas : nekrosis tubulus
fokal, multipel point sepanjang nefron,
skip area, membrane basale ruptur
(tubulo rehexis) lumen oklusi oleh cats
Terdapat pula: kristal hialin eosinofilik
tamm horsfall protein.
Jaringan intersti odem
Regenerasi epitel
Toxic Atn: terutama tub.proximal tersering
MgCl2

Perjalanan Penyakit
Akut Tubuler Nekrosis :
1. Initiating:36 jam urine rendah sedikit (oliguria)
2. Maintenance stage:oliguria 40-400ml
Garam
Air

Tubulo interstitial nephrosis

Krsk TUB

Intersti

Pielonefritis Akut

Inflam supuratif akut

Inf bakt
Hematogen
Penyebaran septikemi
Ascending
vesico uretral reflux.- kerusakkan pada upper /

lower
Morfol : inflam supp interst pathy - abses pada 1 /2 ginjal
Nekrosis tub. Infitr neutro jar intertsitiel - tub
Khas : Glom resisten thdp infeksi
Bl nekrosis luas dpt - Glom
Komplikasi :1. Nekro. Papil , dgn obstr urin tract
Mikros : Infark nekro koagulatif
2. Pioneprosis #. Abses perinefrik

sembuh Fibros Interst,atropi tub ,infiltrasi limposit

Predisposisi
Predisposisi : 1. Obstruksi Uriner
2. Instrumentasi
3. Vesicoureteric reflux
4. Pregnancy
5. Sex & age
Thn2 pertama laki 2 - meninggi 40 th -
wanita
usia ---BPH
6. Lesi primer - Jar parut intra renal
obstruksi
7. DM tindakan kateter
8. Imunosupresi & imunodefisiensi

Klinik :
Akut : nyeri kostovertebral
demam, malaise
disuria
Urine : Pus . Bakteri(E. Coli .Pseudomonas.
Strep. Faecalis ) , RBC, protein ,
darah

Pielonefritis chronik

CPN : merupakan inflamasi tubulo interstitial

chr
Jar parut kel calykes dan pelvis
TDD :
1. Chronic Obstruksi PN
Dpt bilat anomali OBSTR Urin Tract
Unilat Calculi __ Obstruksi unilat
2. Refluk Nefropati VUR ,intra renal reflux
kerusakkan ginjal, atropi, insuf renal chr

Recurrent Infection

Chr . Intersti Inflamasi Urinary obt

End Arteritis

Fibrosis

Stagnation
of urine

Atropi
Parenkhim
Scarring of cortex

Back Pressure

Distort of med
Prog. Obstr Of Nephron
Tu TUBULUS

MORFOL

Jar parut ireg , asimetris

Atropi tub , Hipertr , Dil - tiroidization
Colloud ( protein )
Inflam intersti . CHR
End arteritis obliterasi T sebar
arteriosclerosis hialin tapi glom normal - sp
Focal segmental glomeruloscle
Klinik :1. FG konsentrasi ginjal m hil prog
2. Acidosis 3. RF 4. Hipertensi

Analgetic Abuse Nefropathy

Py Ginj kronik - intake analgetik
Khas : . Nefritis tubulo interstitial chr
Nekrosis papil
Phenacetin , Asoirin - 2 kg > 3 thn , Kafein,
Acetaminophen , Codein
Patogenesis : mula 2 nekrosis papil nefritis
tubulo interstinal cortical
Aspirin Menghambat kerja prostaglandin
ischaemi papil
Klinik : Haedeche , anemi, GIT symptome ,HT
pelvis renalis Pap. Trans .Ca

Urate Nephropathy
Pada Hiperurecemia
1. Acute uric acid Nephropathy
Presipitasi kristal urat pada tub ( Collecting tub )
Obstr nefron ARF
Tu Pada pendrt luekemia, limfoma chemoterapi
INTI SEL HANCUR As urat
2. Chronic uric acid nephropathy / gouty nephropathy
Hiper urecemia Arteri ,Arteriol dd nya tebal
tophus
- Hipertensi

Nephrolithiasis

Hipercalcemia > Hiperparatir

* MM
VIT D intoxikasi
Metastatic bone DIS

Disease of blood vessles

Nefrosklerosis benigna
istilah nyg dipakai pada hpt benigna
hialin arteriosclerosis ischemia fokal
parenkhim penyempitan arteriol
Mrpkan kead khronik 20- 30 thn

Patchy vasc occlution

Stimulation & tr of
Prog Sclerosis -------- un affected glom
Of Glom supplied
Increase filtration
Atropi tub
Tub Dilat
Replacement fibrosis

Cortical Scars

Un affected area
cortex swelling

Granularity of surface

Morfol
Ginjal sdkt mengecil
Cortex sempit
Mikros : Arteri / arteriol lumen sempit -DD tebal & hialinisasi
( prot. Plasma, lipoid, pd membr basalis
Atropi ischemik pathy
1.
Atropi tub, fibr interst
2.

Kerusakk glom
Jrg- insuf ginjal / uremia
GFR N
Prot uri RGN

hiperplasia fibroelastis

Malignant Nephrosclerosis
Malignant / allelarated HT
<-- normotensi

benign HT
sekunder form of ht

Py ginjal lain(glomis /Reflux Nefropati )

Morfol : ukuran ginjal lama py

Hemor kecil - Ruptur arteriol /

glom kap - flea buten

Mikros :
1. Arteriol nekrosis fibrinoid
Arteriolitis Necrotizing
2. Arteri interlobuler
Intima tebal lum
Arteriol
en sempit
- Prol elongated
sel konsentrik ( sel otot
polos )
kolagen konsentrik
arteriolitis hiperplastik onion skinning
renal failure in hioert malig
Kdg Glom nekro
infilt PMN
Kap Trombus ( Necrotizing glomerulitis )

PATOGENESIS
HT malignant : Renin vasokonstriksi
Angiotensin HT
nekrosis
Aldosteron
vasc (injury endotel,Tr .
Nekr fibrinoid. Coagulasi intravasc )
HT Malig : Diast 130 mmHg
Papil edem Retinopati
Ensefalopati
CVS. RF

Morfol
i

OBSTRUKSI

Tiba 2 + komplit GFR sdg

Pelvik + calices dilat
Atropi parenchym kadang 2
Sub total / intermiten GFR tdk
Dil progresif ( tergantung lokalisasi obstr )
Makr : Ginjal > > >, Pelvic + calyc dilatasi
Histol : Atropi tubulus
intersti fibrosis kista 2 ( 15 20 cm )
kortek tipis , piramid obliterasi
Obstruksi : Akut
Unilat , komplit / partial
Bilat partial poliuria , nokturia
Bilat , komplit oliguria , anuria

UROLITHIASIS

> 20 30 thn
Familial
Herediter ( inborn error of metab )
Gout , sistinuria , hiper okaluria primer
ETIOL Patogen :
Tipe 1. Ca ( 75 % ) oxalat fosfat
2., Triple stone ( 15 % ) / Struvite stones Mg
amonium phosphat
3.Uric acid ( 3 % )
4. Cystene ( 2 % )

 Konsentrasi uriner ( vol urin )

Morfol : Renal- Calyc + pelvis

staghorn stone

Perjalanan PY
Ptg obstruksi uriner / ulcerasi bleeding
Batu kecil - Ureter
Besar ----- silent
Excess excretion of stone + Ca
Substance ( oxalate )

lack of urinary
super saturation
fibrinolysis
solution of salt

lack of subtsan keeping

Prot nidus

---------Ca salt in solution (Mg.P)

--------
\

Presipition and
\
Stone formation
\-- lack of inhib of cyistal
formation

Type of renal stone

*Ca ( oxalat , fosfat )

hipercalcemia ,hipercalciuria ( 5% )
hipercalciuria tanpa hipercalcemia ( 15 % )
Absorptive , renal , idiopatik
hiperuricosuria ( 20 % )
hiper oxaluria ( 5 % )
enteric
primary
* Mg ++ , NH3 , Ca , PO4
renal infektion

* Uric acid
~~ hiperuresemia
hiper uricosuria
idiopatik
* Cystine

75%

10 15 %

6%

12%

TUMOR

Benig : ditemukan pada autopsi

jarang menyebabkan gej klinik
Malignan : pada klinik
T. JInak :
Adenoma korteks : kecil, discrete dari tub
ginjal
7-22 % autopsi
Morfol : < 2 cm , kuning abu 2 pucat
discrete , encapsul , nodule
Mikros : Kista papilomatous , sel kuboid / poligonal
tubuler , glanduler , cords , massa undiff

RENAL FIBROMA / HAMARTOMA

< 1 cm , pd autopsi
sel ~ fibroblas
Jar kolagen
ANGIOMIOLIPOMA
ONCOCYTOMA
MALIGNANT TUMOR :
RENAL CELL Ca / HIPERNEFROMA / ADENO Ca
1- 3% T. Ganas viscera 85- 90% dari T.Ganas pd dewasa
T dekade 5 6 : = 3 : 1
Dari Ep Tub ; ~ sigaret
Genetik pd VON HIPPEL LINDAU SYNDR (VHL )
Ditandai ( Hemangioblastoma ssp & Retina ) berkembang Multiple renal
cell Ca

Morfol :
Timbul , dimana saja dr ginjal
p.U nya POOL ATAS
Soliter , unilat , 3 15 cm
Ischemik, nekrosis, fokus hemorragic
Batas tegas, Dgn kapsul renalis
Satelit nodul - agresif
Khas : invasi V. ren ( nod solid ) - V. C. Inf
- jantung

Mikros :
Papiler - solid
clear cell 70 %
Granuler cell ; sarcomatoid pattern --. Prog buruk
well diff ( GRAD I & II )
grade I V
Perjln Py : Klinik nyeri costo vert .masa palpable , hematuria
( 90 % ) : demam, malaise, weak ness , BB menurun
Para Noe plastik syndr ( polisitemia, hiper calcemia ,
Hipertensi dis fingsi hati , feminisasi / maskulin ,
sindr cushing, eosinopilia , Rx lekemoid , amiloidosis

Khas :
Metastase luas sebelum gejala klinik

paru ( . 50 % ) , tulang ( 33 % )
K G B regional , hati , adrenal , 0tak
5 th survival rate 45 %
75 % ( tanpa metastase
jauh ) perinefrik . 15 % - 20 % ( V. Ren )
Th / Nefrektomi

URETER
Kel kongenital :
Double / bifid ; uretero pelvic juntion obstruksi ; divertikel ;
hidro ureter ; megalo ureter
Inflamasi :
Pada urinary tract infeksi :
* Ureteritis folikulris
* Ureteritis cystica
Tumor / tumor like :
Benig T jar mesenchimal
Polip fibro epitelial
Malignan tumor

OBSTRUKSI
INTRINSIK : calculi
Strikctura
Tumor
Blood Clot
Neurogenic
EXTRINSIK : Hamil
Peri ureteral inflam
Endometriosis
Tumor

VESICA URINARIA
Divertikel : kongenital
Accuired
EXSTROPHY :
-- Gangguan perkembangan dinding
ant dan V. URINARIA
Inflamasi :
Cystitis acut & chronis
Pielonef bakterial
Etiologi :
E. Coli ; Proteus ; Klebsiella , entero bacter
TBC, Kandida , Schistosomiasis , Chlamidia , miko plasma

Morfol :
Hiperemi mukosa , Exudat
Hemor. Cystitis
Suppurasi
Ulcerasi
- CHR Folikularis
Eosinofilik
KLINIK :
1. Polalisiria 15 20 %
2. Lower Abdomen pain
3. Disuria

*Sistitis INTERSTITIAL ( Hummers

Cyctitis )
inflam + Fibrosis

Mast Cell
Ulcus
Unknown - Autoimun
* Malakoplakia
- Reaksi inflamasi ---- plak mukosa 3-4 cm
* Metaplasia :
Glanduler ( BRONN S Nest ) - infeksi
Nefrogenik ?
Skuamous
Nonspesific inflam : Batu : RD

NEOPLASIA
Bladder Epithelial Tumor
Benigna
Transtitional cell papilloma
Inverted papilloma
Malignant
Transti . Ca
Grade I
20 %
II , III 60 %
CIS
5- 10 %
Squamous cell ca
Mixed
Undiff . Small cell Ca
Adeno Ca

2-3%
rare
40 %

37%

GRADING TUMOR TGTG DARI

ATIPIA TUMOR

( I ) Some atipia , diff baik

Mitosis jarang
> 7 lapis sel , slight loss of polarity
( II ) Sel tumor msh dikenal dari sel
transitional
> 10 lapis sel
Mitosis > , Greater loss of polarity
Pleomorfik
Bbrp dif skuamosa
( III ) > > ( II )

Keditak teratur nya sus sel Kehilangan &

fragmentasion permukaan sel

Giant cells
sel tent - Flatten ,
Fokus dif . Glanduler

Ca sel skuamosa

Staging :
Description
Marshall stage
------------------------------------------------------non invasive
Papillary
0
CIS
0
Invasive
L. propria
A
Superfis muscle
B1
Deep muscle
B2

Description

Marshall stage

---------------------------------------------------Metastatic
Regional KGB
Distant site

D1
D2

Epidemiologi , Patogenesis :
>3:1
50 -80 thn ( 80 % )
Di lokasi industri , urban
? 1.Industri exposure td arylamines
( 2 naftil amine ) - stlh 15 40 thn
2. Cigarette smoking
3. S. Haematobium 70 % ca squamosa
4. Long time Fenasetin
5.
Cyclofosfamide , imunosupresi agent -- sistitis hemoragik
Ca ( 10 x , set 12 thn )

KLINIK : Hematuria
Prognose : TGTG STAD , GRADE
Grade I : 10 thn survival rate 98 %
II
30 % -- 68 %
Agresif
70 % Ca Squamosa
T. C. C
Papillary
Flat lesion
Non invasive
invasive

Grading I papiler

II papiler / flat
III papiler , flat ,
fungating.
nekrosis ,
ulserasi
invasi ---- otot
Mesenchimal tumor & sekundary tumor

Uretra :

Inflamasi
Tumor
Caruncle - inflamasi
Papilloma
Carsinoma

PROSTAT

Inflamasi :
Prostatitis bakterial akut
Khronik
Prostatitis abakterial khronik

Prost. bakt akut

Prost.bakt.khronik

Inflam. Supp.fokal/

UTI : E. coli
gram (-),entero
kok,staf.
V. uri
-- intraprost
Uretra post reflux of urine
Limfo hematogen. Distant foci
inflamasi kronik
Kateterisasi, sitoskopi, dilat uret
Prosedur reseksi prostat
D/ kultur, klinik
Morfol inflamasi (abses)

UTI recurrent (sisti

tis,uretritis )
serangan acut (-)
D/ sukar
Klinik : low back
pain.disuri
discomfort supra
pubic.perineal
morfologi

PROSTATITIS ABAKTERI
KRONIK

KLINIK : sukar dibedakan prost bakt

kronik
Riwayat UTI rekurens (-)
15 leukosit/lap pandang, kultur (-)
Laki2 seksual aktif klamidia trachomatis
urea plasma
urealyticum

prostate specific antigen may be slightly elevated.

This is chronic prostatitis. Numerous small dark blue lymphocytes are seen in
the stroma between the glands. There may be a bacterial agent accompanying
this inflammation, and cystitis or urethritis may also be present. However,
more commonly, chronic prostatitis is abacterial and there is no history of
urinary tract infection. The serum

NODULER HYPERPLASIA

Benign prostatic hypertropi/ hiperplasia

periuretra obstruksi uretra
Insiden : 20% laki2, 40 th,
70% laki2 60 th
90% 80 th
nod hyperplasia is not truly a disease /
a normal aging
Etiologi : unknown
? Berhub aksion androgen

Testosteron --------- dihidrotestosteron

5 reduktase
mediator prost growth
autosomal ressesive ------ perkembangan
prostat terganggu (5 reduktase defisiensi)

Akumulasi DHT hiperplasia

Klinik
morfologi

KARSINOMA

sering setelang lung cancer

Penyebab kematian kedua
200.000 kasus baru 1/5
Insidens laki2 >50th
Etiologi: risk factor: age, race, family history, genetik
cromosome 8-10-16, level hormone, environmental
Morfologi : 70% periferal zone, tu: post
Khas : T pasir, firm
bila bercampur dg subs prostat sukar di D/
palpasi (+)

SREAD

Lokal invasive : vesika seminalis, VU

obstruksi urinair
Hematogen : tulang (axial skeleton,
viscera)
osteolitik (lumbar, spine,
femur prok, pelvis, thorax spine, ribs)
Limfogen : KGB obturator, perivesikal,
hipogastrik, illiac, presakral, paraaorta

Histol :

Glandul ,kecil,/ medium ,single

layer.kuboid / torak
Papiler, Cribriform
Cord,nest,sheet
besar---vakuol
Back to back
(well
anak inti
dif BHP)
Mitosis ---- extremely un common

Mikros :

Large gland intra acini prol. Early

- inti anaplastik
- sel displastik dikelilingi lap
sel
basal
- membrana basalis intak
Grading penting --- prognose dan der
diff

STAGE A :

Mikr : not clinically palpable T

A1 focus < 5% of tissue eximined low
grade
A2 multiple area > 5% (gleason grade
>4)

STAGE B

Makroskopis : palpable makroskopis tumor

B1 < 1,5cm, only one lobe
B2 > 1,5 cm, or several
nodules inboth lobes

STAGE C

Tumor with extracapsuler extension but

still clinically localized
C1 palpably extending into seminal
vesicle, no fixed to pelvic wall
C2 fixed to pelvic wall

STAGE D

Metastasic tumor
D1 metas terbatas pada 3 KGB
pelvis/fewer
D2 > KGB / metas extra pelvis (tulang)
TNM staging for local tumor - roman I
s/d IV

PERJALANAN PENYAKIT

Stage A : meningkat sesuai dg usia 60 % 80 th

Mikroskopis cancer ditemukan pd otopsi / TUR BHP
Stage A progresif (-) (10 th) 5-25%-lokal / metas
Pada usia muda yg HPP lama (<60th)
A2 30-50 % progresive dalam 5 th 20% untreated
Stage B 5-10 % kel urin (-) RT (+)
tumor pada subkapsul

Stage C,D 75 % kel urinair sukar mulai

/ stop uriner, disuri / hematuri,
polakisuri
Nyeri perineal
Stage D : back pain metastasis
vertebra osteoblastik metastasis
PSA ?