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1.Massive proteinuria, with the daily loss of 3.5 gm or more of protein (less in
children).
3.Generalized edema
• It is the most common cause of acute renal failure which signifies rapid
reduction of renal function and urine flow, falling within 24 hours to less
than 400 mL per day.
Causes:
• Ischemia
• There are two routes by which bacteria can reach the kidneys:
(1) through the bloodstream (hematogenous infection) and (2)
from the lower urinary tract (ascending infection)
•Acute pyelonephritis is an acute suppurative inflammation of the kidney caused by
bacterial and sometimes viral (e.g., polyomavirus) infection, whether hematogenous
and induced by septicemic spread or ascending and associated with vesicoureteral
reflux.
Morphology :
• The tubules show atrophy in some areas and hypertrophy or dilation in others. Dilated tubules with flattened epithelium may
be filled with colloid casts (thyroidization). There are varying degrees of chronic interstitial inflammation and fibrosis in the
cortex and medulla. In the presence of active infection there may be neutrophils in the interstitium and pus casts in the
tubules. Arcuate and interlobular vessels demonstrate obliterative intimal sclerosis in the scarred areas; and in the presence
of hypertension, hyaline arteriosclerosis is seen in the entire kidney. There is often fibrosis around the calyceal epithelium as
well as a marked chronic inflammatory infiltrate. Glomeruli may appear normal except for periglomerular fibrosis, or exhibit a
variety of changes, including ischemic fibrous obliteration and secondary changes related to hypertension.
Vascular Diseases
Congenital Abnormalities
Horseshoe kidney:
•Cystic diseases of the kidney are heterogeneous, comprising hereditary, developmental, and
acquired disorders.
Clinical course:
•The enlarged kidneys, usually apparent on abdominal palpation, may induce a dragging
sensation.
•The disease occasionally begins with the insidious onset of hematuria, followed by other
features of progressive chronic kidney disease, such as proteinuria (rarely more than 2
gm/day), polyuria, and hypertension
• Morphology. In gross appearance, the kidneys are usually bilaterally
enlarged and may achieve enormous sizes; weights as high as 4 kg for
each kidney have been reported. The external surface appears to be
composed solely of a mass of cysts, up to 3 to 4 cm in diameter, with
no intervening parenchyma.
Microscopic examination
•The cysts may be filled with a clear, serous fluid or, more usually, with
turbid, red to brown, sometimes hemorrhagic fluid.
•As these cysts enlarge, they may encroach on the calyces and pelvis to
produce pressure defects.
•The cysts arise from the tubules throughout the nephron and therefore have
variable lining epithelia.
•On occasion, papillary epithelial formations and polyps project into the
lumen. Bowman capsules are occasionally involved in cyst formation, and
glomerular tufts may be seen within the cystic space.
Urinary obstruction
• Obstruction increases susceptibility to infection and to stone
formation, and unrelieved obstruction almost always leads to
permanent renal atrophy, termed hydronephrosis or obstructive
uropathy.
• May occur at any level of the urinary tract from the urethra to
the renal pelvis.
1.Congenital anomalies: posterior urethral valves and urethral strictures, meatal stenosis, bladder
neck obstruction; ureteropelvic junction narrowing or obstruction; severe vesicoureteral reflux
2.Urinary calculi
7.Pregnancy
9.Functional disorders: neurogenic (spinal cord damage or diabetic nephropathy) and other
functional abnormalities of the ureter or bladder (often termed dysfunctional obstruction)
Hydronephrosis
• Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney
due to obstruction to the outflow of urine
• The kidney may be slightly to massively enlarged, depending on the degree and the
duration of the obstruction.
• The earlier features are those of simple dilation of the pelvis and calyces, but in addition
there is often significant interstitial inflammation, even in the absence of infection.
• In chronic cases the picture is one of cortical tubular atrophy with marked diffuse
interstitial fibrosis. Progressive blunting of the apices of the pyramids occurs, and these
eventually become cupped.
• In far-advanced cases the kidney may become transformed into a thin-walled cystic
structure having a diameter of up to 15 to 20 cm with striking parenchymal atrophy, total
obliteration of the pyramids, and thinning of the cortex.
Clinical course
• They may be present without producing any symptoms or they may cause
significant renal damage.
• In general, smaller stones are most hazardous, because they may pass
into the ureters, producing colic, one of the most intense forms of pain, and
ureteral obstruction.
• Larger stones cannot enter the ureters and are more likely to remain silent
within the renal pelvis. Commonly, these larger stones first manifest
themselves by hematuria. Stones also predispose to superimposed
infection, both by their obstructive nature and by the trauma they produce.
Morphology. Stones are unilateral in about 80% of patients. The favored sites for
their formation are within the renal calyces and pelves and in the bladder. If formed
in the renal pelvis they tend to remain small, having an average diameter of 2 to 3
mm. These may have smooth contours or may take the form of an irregular, jagged
mass of spicules. Often many stones are found within one kidney.
Tumor of Kidney
• The tumors occur most often in older individuals, usually in the sixth and
seventh decades of life, and show a 2 : 1 male preponderance.
• Because of their gross yellow color and the resemblance of the tumor
cells to clear cells of the adrenal cortex, they were at one time called
hypernephroma. It is now clear that all these tumors arise from tubular
epithelium and are therefore renal adenocarcinomas.
• The peak incidence for Wilms tumor is between 2 and 5 years of age, and
95% of tumors occur before the age of 10 years.
The classic triphasic combination of blastemal, stromal, and epithelial cell.Sheets of small
blue cells with few distinctive features characterize the blastemal component. Epithelial
differentiation is usually in the form of abortive tubules or glomeruli. Stromal cells are
usually fibrocytic or myxoid in nature, although skeletal muscle differentiation is not
uncommon.
ANATOMI
KELAINAN KONGENITAL
HIPOSPADIA
Hipospadia
orifisium uretra yang
abnormal disepanjang
aspek ventral penis
1 dari 300 kelahiran
hidup bayi laki-laki
EPISPADIA
Epispadia
Orifisium uretra di
aspek dorsal penis
FIMOSIS
Mikroskopis:
Epidermis yang tipis dan
kadang-kadang ulcerasi disertai
infiltrat padat limfosit dan sel plasma
Pembuluh darah mengalami hipertrofi
dan proliferasi sel endotel, infiltrasi sel
inflamasi di dinding pembuluh darah
Spirochetes dapat ditunjukkan dengan
pengecatan Warthin-Starry silver stain
TUMOR
Condyloma acuminatum
Penyakit menular seksual
yg disebabkan HPV tipe 6
kadang2 tipe 11
Pertumbuhan pedunculated,
sessile, papiler merah pd meatus
penis atau fossa navicularis
atau bagian lain di glans penis
Condyloma acuminatum, low power.
BOWENOID
Bowen disease PAPULOSIS
BOWEN DISEASE
Secara Histologi
bowenoid papulosis tidak dapat
dibedakan dengan Bowen disease
terkait dengan HPV type 16.
The boundaries between stroma Deeply invasive carcinomas may focally show spindle,
and tumour are irregular or finger pleomorphic, acantholytic, giant, basaloid or clear cells.
like.
SCROTUM
LESI NON NEOPLASTIK
HIDROKEL
Akumulasi cairan serosa dalam tunika vaginalis
Akumulasi darah (hematokel), cairan limfe (kilokel)
Bedakan spermatocele (asal epididimis) ada sperma
dalam cairan kista.
Outer appearance of hydrocele. The wall is translucent and the content had a serous quality.
NEOPLASMA
Seminoma
A. Low magnification shows clear seminoma cells divided into poorly demarcated lobules by
delicate septa.
B. Microscopic examination : large cells with distinct cell borders, pale nuclei, prominent
nucleoli, and a sparse lymphocytic infiltrate. Cells are large, round-polyhedral with distinct
cell membranes, abundant clear/watery cytoplasm (glycogen), large central nuclei, 1-2
prominent often elongated and irregular nucleoli. Usually minimal mitotic figures.
Granulomatous inflammation with Langhans type multinucleated giant cells present in
20%
Yolk Sac Tumor
• Tumor testis yang paling sering terjadi pada bayi dan anak-
anak < 3 tahun
• 50% tumor dapat terlihat endodermal sinuses (Schiller-Duval
Bodies): inti mesodermal dengan papiler di tengah dan lapisal
sel visceral dan parietal seperti glomelurus primitif
• Schiller–Duval bodies mirip dengan glomelurus, mempunyai
inti mesodermal dengan papiler di tengah, dilapisi oleh sel
pipih baik sel visceral dan sel parietal
• Adanya PAS dan AFP staining positif untuk hialin globul
Germ Cell tumor (GCT) Non Seminomatous tumor
Primitive tumor cells, which are relatively small and less pleomorphic relative to embryonal carcinoma.
Majority cases of these tumors is microcystic structure, which is characterized by the presence of a
spider-weblike network formed by vacuolated cytoplasm of tumor cells, similar to a honeycomb.
Schiller Duval bodies (Yolk sac tumor)
• Terkadang berhubungan
dengan ginekomastia
• Melepaskan hormon
androgen ,estrogen
• Sebagian besar bersifat
jinak
• 10% Metastasis
• Mitosis
• Pleomorphis
• Ukuran sel besar
• Nekrosis
Tumor sel sertoli
sel tumor tersusun dalam trabekula yang membentuk struktur tali(cord) dan tubulus
LIMFOMA TESTIS
• 1. INFLAMASI
• 2. HIPERTROFI NODULAR JINAK→ >>
• 3. TUMOR
1. INFLAMASI
Prostatitis bakterialis akut
Prostatitis bakterialis kronik
Prostatitis non-bakterialis kronik
Prostatitis granulomatosa
PROSTATITIS BAKTERIAL AKUT
- >> Karena E.coli
- biasanya akibat intraprostatik reflux urin
dari uretra posterior atau kandung kemih,
bisa juga merupakan penyebaran
limpohematogen dari fokus infeksi yang jauh
- akibat dari manipulasi pada uretra atau prostat
(kateterisasi,cystoscopy,dilatasi uretra, reseksi
prostat)
PROSTATITIS BAKTERIAL AKUT
• Gejala klinis prostatitis bakterial akut berupa
panas, disuria, menggigil.
• Pemeriksaan prostat : lembek,nyeri tekan
• Diagnosis : kultur urin dan pemeriksaan klinis
PROSTATITIS BAKTERIAL AKUT
Infiltrat radang dalam lumen, area nekrosis, stroma sembab (gambaran abses)
PROSTATITIS BAKTERIAL KRONIS
• Genetik
• Allelic lost pada tumor suppressor gene (8p, 10q, 13 q, 16q dan 17p)
• Fusi TMPRSS2 gene dan ETS transcription factor gene (ERG)
• Gene silencing (PTEN, RB, p16/INK4a, MLH1, MSH2 dan APC).
• Ras
Banyak di derita ras Afroamerican
• Diet
Diet tinggi lemak hewani
• Hormonal
Tidak terjadi pada laki-laki yang dikastrasi sbl pubertas atau
pada populasi dengan ekskresi rendah-5 alpa-reductase,
insidensinya sangat rendah
• Aktivitas seksual
Seksual aktivitas yang dini, mempunyai banyak partner sex,
meningkatkan insidensi, kemungkinan infeksi STD dan ekses
dari testosterone
• Hipotesa viral infeksi
Sejak thn 1970, herves virus dicurigai, tapi blm ada konfirmasi
• Lingkungan.
Radiasi gamma, konsentrasi kadmium yg tinggi.
Grossly, the tumor may be difficult to see but usually can be identified as a gray or
yellowish, poorly delineated, firm area
Histopatologi adenokarsinoma prostat