Tractus urinarius

Dr.Resmi Kartini
 KERUSAKAN GLOMERULUS
1.Out put urin menurun
2.Proteinuria
3.Hematuria
Swelling of endothel inflamation
altering focal
loss of
Blood flow permeability
epithelium
of layer +
endotel

Urin proteinuria
hematuria
 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. Urine : protein,red ceels,hb,pmn

2. 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 Pre renal ( perdarahan,shock,Vol deplet

Renal ion ,congestive heart failure )

Disorder
- kerusakkan parenkhim ginjal (-)

Post renal obstruksi

gejala klinik
Uremia
Biokimia aqbnormal
 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 Altered Fluid

EGM matrik cell growth secretion

Cyst
 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

4. Adult onset medullary cystic dis ( 15 % )

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 ? Planted Ag

tipe A Ag A b glom circulating

complek imun compl

(faring, kulit ) * cytoplasmic AG
( endostreptosin )
* cationik AG
*Proteinase ( strep

Erythrogenic toxic )
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 lumen kapiler
obliterasi

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 focal increase escape of
Stimulation diminised in permeabilitas red
cell
of juxta filtration fluid
glom App retention
oliguria

Rise in blood rised oedema unselektif

hematuria
Pressure blood urea protein urea

Casts

epithelial protein red cells

 PERJALANAN PENYAKIT
ACUTE DIFFUSE ( PROL ) G.N

CARDIAC FAILURE MILD PROTEIN PERSISTING RAPIDLY

OR UREMIA PERSISTING FOR PROTEINURIA PROG.
G.N
MONT OR TWO 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% CGN
RPGN 40%
MGN 50%
F.G sklerosis 50-80%
MPGN 50%
IgA 30-50%
others
 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
Nefrotoxic
Ep tubulus sensitif thdp anoxia, toxin
injury

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
Atropi of urine
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 hiperplasia fibroelastis

Jrg- insuf ginjal / uremia

GFR N
Prot uri RGN
 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 ) 75%
hipercalcemia ,hipercalciuria ( 5% )
hipercalciuria tanpa hipercalcemia ( 15 % )
Absorptive , renal , idiopatik
hiperuricosuria ( 20 % )
hiper oxaluria ( 5 % )
enteric
primary
* Mg ++ , NH3 , Ca , PO4 10 15 %
renal infektion
* Uric acid 6%
~~ hiperuresemia
hiper uricosuria
idiopatik
* Cystine 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 2 - 3 %
Inverted papilloma rare
Malignant
Transti . Ca 40 %
Grade I 20 %
II , III 60 %
CIS 5- 10 %
Squamous cell ca 37%
Mixed
Undiff . Small cell Ca
Adeno Ca
 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 , Ca sel skuamosa
Fokus dif . Glanduler
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 D1
Distant site 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 recurrent (sisti
tis,uretritis )
UTI : E. coli serangan acut (-)
gram (-),entero D/ sukar
kok,staf. Klinik : low back
V. uri pain.disuri
-- intraprost discomfort supra
Uretra post reflux of urine pubic.perineal
Limfo hematogen. Distant foci morfologi inflamasi
kronik
Kateterisasi, sitoskopi, dilat uret
Prosedur reseksi prostat
D/ kultur, klinik
Morfol inflamasi (abses)
 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 ?