GINJAL

&
SALURAN
KEMIH

Dr. T. Ibnu Alferraly, SpPA

Departemen Patologi Anatomi
Fakultas Kedokteran – USU / UISU
2008
 Spe cif ic Fu nct ion of
Ki dney
• Filtering Wastes From Blood Plasma
 The kidneys filter blood plasma out of the
bloodstream and remove its undesirable
substances to produce urine.
 The kidneys filter about 180 quarts of blood plasma out of the
bloodstream each day.
 About 99% of this blood plasma (minus most of the wastes) is
reabsorbed by the kidneys to reduce urine production to about 1
to 2 quarts each day.
 Without functioning kidneys, wastes accumulate in the blood
causing a serious condition called "uremic poisoning" or "uremia."
 Kidneys are also responsible for regulating the acidity of the blood
by excreting alkaline salts when necessary.
Kidneys :

• retroperitoneum ; 130 – 150 gr each

• surface smooth, capsule (+), surrounded perinephric fat + Gerota’s fascia
• anatomic unit : NEPHRON = glomerulus, proximal convulated tubule, loop
of Henle, tubules
• 1 kidneys = 1 million nephrons

Renal Functions

• Glomerular Filtration
GFR normal : 120 ml / min, measured by : the clearence of exo –
genous inulin ( Inulin Clearance Test ) or endogenous creatinine
( Creatinine Clearance )

• Tubular Reabsorption
Ur in e F orma tion

 Glomerular filtration
 Tubular reabsorption
 Tubular secretion

 Urinary excretion :
glomerular filtration + tubular secretion
- tubular reabsorption
The normal renal cortex contains glomeruli, other vessels, tubules and
interstitium. When evaluating a renal specimen by light microscopy on
an H&E stained section
In the glomerular diagram,
The different colors indicate the
various cell types that are of interest
in assessing the pathologic changes
that occur in a glomerulus
(green = epithelial cells, yellow =
endothelial cells, red = mesangial
cells).
Special stains that often are used in evaluating renal biopsy
specimensI from left to right: PAS, trichrome, H&E, Jones silver stains).
Diagram of a single glomerular capillary and illustrates the ultrastructural
features that are assessed when evaluating renal biopsy specimens.
Electron micrograph that shows a portion of 1 capillary loop with
adjacent mesangium
Much higher magnification electron micrograph.
The urinary space and the foot processes are at the top.
Gejala Klinis Penyakit Ginjal :
• Sakit
- Parenkhim ginjal : tanpa ujung saraf rasa sakit
- Rasa sakit Ok :
> Meregangnya fascia ginjal
> KOntraksi otot ureter : pd obstruksi ( urethral collic )

• Hematuria
- Dengan / tanpa rasa sakit
- Severe : urin merah, tkt rendah : tidak terlihat, tetqpi dengan mikr’kop
pd sedimen urin eritrosit (+)
- Penyebab :
> Penyakit Ginjal : glomerulonefritis, pyelonefritis, neoplasma,
trauma, calculi, dll
> Penyakit2 pada kndung kemih, ureter, uretra : cystitis, uretri-
tis, calculi, dll
> Penyakit sistemik yg menyebabkan perdarahan saluran
kemih : malignant hypertension, emboli sistemik pd endo –
karditis, diathesis, terapi antokoagulan,
Osler-Weber-Randu Diseade
Proteinuria

• Sangat bermanfaat utk screening peny ginjal

• Bbrp individu : orthostatic / exercise proteinuria

Pyuria
Adanya neutrofil pd urin

Sindroma nefrotik
> 3,5 gr/d + hipoproteinemia + edema

Nefritis Akut ( Acute Nephritic Syndrome )

oliguria ( < 700 ml/d ) + hematuria + proteinuria + hipertensi +
azotemia

Gagal Ginjal ( acute / chronic )

Hipertensi
Pemeriksaan :

• Fisik diagnostik
• Radiologi
- foto abdomen polos
- intravenous pyelography
- ultrasonography
- renal arteriography

• Pemeriksaan urin
• Pemeriksaan darah
• Biopsi ginjal
Kelainan Ginjal Kongenital

• Renal Agenesis ( unilateral or lateral )

• Renal Hypoplasia : ginjal < 50 gr pd dewasa
• Ectopic Kidney : dapat sebabkan obstruksi dan infeksi
• Horshoe Kidney
• Renal Dysgenesis ( Displasia Ginjal )

Kelainan Kistik Ginjal :

• Adult Policistic Disease

• Infantile Polycistic Disease
• Medullary Cystic Disease
• Glomerulocystic Disease
• Simple Renal Cysts
• Dialysis Cystic Disease
Clinical Presentations of Glomerular Diseases

Clinical Manifestations of Glomerular Disease

•asymptomatic proteinuria
•nephrotic syndrome
(proteinuria, hypoproteinemia, hyperlipidemia, edema)
•asymptomatic hematuria
•glomerulonephritis
(hematuria, proteinuria, hypertension, renal failure)
•acute glomerulonephritis
(neprhitis with short term renal failure)
•crescentic glomerulonephritis
(nephritis with rapidly progressive renal failure)
•chronic glomerulonephritis
(chronic progression of renal failure)
•End Stage Renal Disease
(irreversible renal failure)
Penyakit Yang Terutama Mengenai Glomerulus
 Glomerulonefritis proliferatif
 kelainan minimal
 nefropati mebranosa (epimembranosa atau
ekstramembranosa).
 glomerulosklerosis fokal
 glomerulonefritis menahun (khronik)
• Glomerulonephritis fokal yang mungkin berasal imunologik, tetapi bukan
oleh infeksi sistemik
Kelainan itu secara klinik dibagi atas :
- glomerulonephritis fokal idiopatik,
- hematuria recurrens
- kerusakan ginjal sebagai bagian penyakit komplex imun
sistemik seperti lupus erythematosus, periarteritis
nodosa, dan purpura Schonelein-Henoch (purpura
anafilaktoid).
PENYAKIT – PENYAKIT GLOMERULUS :
Glomerulonephritis acute.
Etio : Streptococcus
Virus
Staphylococcus
Pneumococcus
Patogenesis :
* Biasanya didahului oleh infeksi ISPA, tonsi -
litis, pharingitis, otitis, mastoiditis, infeksi
kulit.
* Kemudian timbul reaksi agab
* Agab complex melekat ke glomerulus menim
bulkan reaksi radang terutama pada membran
basalis glomerulus
* Glomerulus kehilangan foot processus

Klinis : - Edema pada muka & peri orbital

- Edema bisa ke tangkai bawah
- Malaise, demam
- Mual muntah
- Oliguria, proteinuria, hematuria
- Hipertensi
Makroskopik :
> Glomerulus hipertrofi dan hiperselular dan proliferasi
> Sebukan sel-sel radang
> Nekrosis fibrinoid dinding kapiler
> Penebalan membrane basalis

Etiologi :
* Sindroma neprotik primer ok. Glomerulopati
* Sindroma neprotik secunder akibat :
- Penyakit-penyakit sistemik misalnya : DM.
Amiloidosis,lupus, Hodgkin, dsb
- Gangguan sirkulasi darah trombosis vena renalis
D.C
- Keracunan : logam berat, obat-obatan, gigitan ular,
lebah
- Infeksi/parasit : sipilis,malaria
- Genetik, familial

Patogenesis :

Perubahan pada membrane basalis kapiler glomerulus

Permeabilitas protein dan albumin bertambah.
NEFROSIS

Merupakan kelainan ginjal degeneratif yang terutama mengenai

tubulus :

I.Acute Tubular Necrosis:

A. Nefrosis toksik
- Nefrosis kimiawi
- Nefrosis cholemik
- Nefrosis osmotic
- Nefrosis vakuoler
B. Nefrosis hipoksik

II. Nefrosis kronik

P Y E LO N E F R I T I S

Radang ginjal yang mengenai parenchyma dan pelvis.

Infeksi dari : > Hematogen dari Tonsilitis Septikemi

> Ascenden dari kandung kemih , dll
> Limfatik

Faktor – faktor predisposisi :

- Obstruksi air kemih
- Kehamilan
- Instrument
- Penyakit Syaraf, paraphelia, poliomielitis
- D.M
- Daya tahan turun

Klinis : - Demam tinggi

- Nyeri diatas ginjal
- Leukositosis
HIDRONEFRITIS
Terjadinya dilatasi pelvis renalis dan calyces, serta atrofi progresif
dan pembentukan kistik ginjal disertai pelebaran ureter.

Etiologi Hidroneprosis :
1. Obstruksi :
Ureter : batu , tumor
Dinding ureter : striktura
Penekenan dari luar : tumor, prostat hiper
tropi, fibrosis

2.Kelainan neuromuskuler : Paraplegi, sclerosis multiple,

tabes dorsalis
3.Kehamilan
4.Idiopatik

Klinis :
Nyeri pinggang
Teraba tumor pada sudut costo vertebral.
Payah ginjal
Pyelonephritis
Makroskopis : - Kortex menipis dan atrofi
- Ginjal membesar
- Pelvis dan calyces melebar

Mikroskopis : - Dilatasi tubulus

- Atrofi tubulus
- Glomerulus atrofi & fibrosis

UROLITIASIS

Adalah : pembentukan batu dalam saluran kemih dan penyakit yang

berhubungan dengan adanya batu tersebut.

Faktor Predisposisi :
> Konsentrasi kristaloid dalam urine
> Lesi pada dinding tract.urinarius atau perubahan
fisiokimiawi air kemih
> Stasis urine
Misalnya :
1.Dehidrasi
2.Hiperkalsemia, hipercalciuria pada hiperparathyroid,
resopsi tulang, hipervitaminosis D, diet calcium meninggi,
antasida.
3.Penyakit-penyakit gout
4.pH kurang dari 6
5.Defisiensi Vit. A
6.Infeksi kuman, parasit

Klinis :
Ulserasi dan perdarahan
Colic ginjal / ureter
Pyelonephritis, cystitis
Hidronephrosis
Carcinoma
Jenis2 Batu Sqaluran Kemih
Br oad classi ficati on

 Calcium containing stones

 75%
 Radiopaque

 Non calcium containing stones

 25%
 Radiolucent
 Not cystine stones are radiopaque (sulphur)
Risk Factors for Calcium Stone-Formation

Age
Gender
Season/climate
Fluid Intake
Stress/diet
Occupation
Mobility
Metabolic disorders
Genetic disorders
Anatomical abnormality
Family history
 Occupation, Low Urine Volume and Urolithiasis

Occupation Percent of Male Urine

Stone-Formers Volume
(litre/day)

Taxi-Drivers, Chauffeurs 5.6 1.42 ± 0.27

Chefs, Kitchen-Workers 6.3 1.31 ± 0.34

 Urinary Risk Factors for Stone-Formation

• Low urine volume (<1L/24hrs)

• Alteration in urinary pH (<5.5,>7.5)
• Hypercalciuria (>4mg/kg/24hrs)
• Hyperoxaluria (45mg/24hrs)
• Hyperuricosuria (>600mg/24hrs)
• Hypocitraturia (<250mg/24hrs)
• Hypomagnesiuria (<50mg/24hrs)
TUMOR GINJAL
Jinak : Adenoma Ganas : Karsinoma
Fibroma Tumor Wilms
Myxoma ,dsb Fibrosarcoma,dsb

1.Karsinoma sel ginjal (Renal Cell Ca : tumor Grawitz, hypernephroma, clear

cell carcinoma)
berasal dari epitel tubulus

Makros : - Massa besar, berlobus-lobus

- Massa kuning
- Sebagian bercapsul
- Tampak daerah nekrosis dan perdarahan

Mikros : - Kelompokan sel-sel besar

- Sel dengan sitoplasma jernih
- Clear cell
2. Tumor Wilms : ( Nephroblastoma, Carcinoma )
Biasanya mengenai anak-anak.

Makros : Tumor putih kelabu seperti otak, lemak

Mikros : - Glomelurus abortive
- Stroma spindle
Signs and Symptoms

 Hematuria  Liver dysfunction

 Fever  Hypercalcemia
 Weight loss  Incidental finding of
 Erythrocytosis lytic lesions on
routine chest x-ray
RCC ( Renal Cell Carcinoma )
 In 2003 31,900 new cases
RCC were expected in the
U.S., with 11,900 deaths
attributable to RCC

 Classic triad: flank pain,

hematuria, palpable mass

 Paraneoplastic
syndromes: erythrocytosis,
hypercalcemia
Backgro un
d
 Higher incidence in cigarette smokers

 Associated with Von Hippel Lindau disease, which is caused

by mutations in chromosome 3

 Frequently invades renal veins or IVC leading to hematogenous

dissemination

Prognosis (Young, et al 2003)

 UCLA researchers described a staging system based on TNM stage,
histologic grade, and performance status

 This system predicts the clinical outcome and survival for patients who
had surgical resection of their kidney tumor

 Patients are assigned to low-, intermediate-, and high-risk groups

based on these 3 variables
 Pro gnosis

5 year survival ranges (UCLA):

Nonmetastatic / low-risk = 83.8%

Nonmetastatic / high-risk = 44%

Metastatic / high-risk = 0%
 Prognosi s (Rathmell 2004)

 Patients with clear cell RCC had a poorer prognosis

than those with either papillary or sarcomatoid RCC
 5-year survival rates:
 68.9% clear cell
 87.4% papillary
 86.7% sarcomatoid

 Currently researchers are trying to identify Rx for each

specific subtype of RCC, since the underlying genetic
changes are unique to each subtype
Sta ging
 Tx Primary tumor cannot be assessed.

 TC No evidence of primary tumor.

 T1 Tumor less than 7 cms in greatest dimension limited to

the kidney.

 T2 Tumor more than 7 cms in greatest dimension limited to

the kidney.

 T3 Tumor extends into major veins or invades adrenal

gland or perinephric tissue but not beyond Greota’s fascia.
Criteria fo r Nephre ctomy

 > 75% tumor debulking possible

 No CNS, liver, or bone mets

 Adequate pulmonary and cardiac function

 Good performance status

 Biopsy with clear cell type

Wilm’s
Tumor
Wilm’s
Tumor
 KANDUNG KEMIH
Radang = Cystitis

Faktor Predisposisi : - Obstruksi air kemih

- Trauma instrument
- Pyelonephritis
- Batu vesica urinaria
- Cystocele
- D.M
- Septikhemia

Klinis :Pollakisuria, Dysuria, Nyeri supra pubis, Gejala sis-

temik : demam,dsb

Tumor Jinak : Papilloma

Tumor Ganas : Karsinoma (terutama jenis transtitional)
Karsinoma Skuamous
Blader Neck Obstruction
O.K.Penyempitan muara uretha : * Hipertrofi prostate
* Karsinoma
* Fibrosis ok.cystitis chronica
* Benda asing
Batu kandung kemih :
- Primer
- Sekunder
Faktor predisposisi :
> Retensi urine
> Infeksi bakteri
> Benda asing
> Vit. A defisensi

Neurogenic Bladder : Kandungan kemih yang kehilangan fungsinya

akibat terputusnya persyarafan

Gejala : > Inkontinensia urine

> Autonomic neurogenic bladder : keluarnya urine karena
kandung kemih telah penuh.
BLADDER C ANC ER

Incidence
There are approximately 55,000 new cases of bladder, ureter and renal
pelvis cancers in the United States with approximately over 13,000
deaths each year.

Epidemiology

 Gender
 Men have more incidence of bladder cancer than women and
increased incidence in 7th decade of life.

 Race
 Cancers are more common in whites than blacks – 2:1.
Etiology and Risk Fact ors

 Cigarette smoking
 Analgesic abuse
 Analgesic compounds, especially Phenacetin, has been
associated with increased risk of bladder cancer
 Chronic urinary inflammation
 Occupational exposures
 Workers with organic chemicals, rubber, paint, and dye
industries have increased risks of urothelial cancers.

 Balkan nephropathy
 Increase of cancer with renal pelvis and ureters in patients in
Balkan nephropathy, unknown cause that results in
progressive inflammation of the renal parenchyma
 Genetic factors
 Families with higher risk of transitional cell carcinoma, no
genetic basis has been found as of yet
Si gns and Sym ptoms
 Hematuria
 Urinary voiding symptoms
 Symptoms of advanced disease usually involve swelling in lower
extremities secondary to a lymphatic obstruction
 Pain and frank hematuria

Diagnostic Work-up
 CT scan
 Ultrasound
 Intravenous pyelogram
 Urine cytology from both ureters at time of cystoscopy
 Bone scan
 Chest x-ray
Pathol ogy

 Transitional cell carcinoma constitutes 90-95% of

bladder, ureter and renal pelvis cancers.

 Squamous cell carcinoma up to 7%

 Adenocarcinoma, rare, less than 3%

 Adenocarcinoma in the bladder which arises from the dome is
felt to be urachal in origin.

 Carcinoma in situ 30% of newly diagnosed bladder

cancer with multiple sites of bladder involvement
TNM S tag in g

 TX Definition – Primary tumor cannot be

assessed

 T10 No evidence of primary tumor

 TA Noninvasive papillary tumor

 Tis Carcinoma in situ flat tumor

 T1 Tumor in wedge
Subepithelial connective tissue

 T2 Tumor in wedge muscle

T2a tumor in wedge, superficial
muscle, inner half
T2a tumor in wedge, deep
muscle, outer half
Prognosti c Factor

 Lesions up to T1, especially TA, without carcinoma in situ have

95% survival rate whereas those with high grade T1 lesion have a
10-year survival rate of 50%.

 Muscle invasive carcinoma 5-year survival rates are 20-50%.

With regional lymph node involvement 5-year survival rate is 0-
20%.