URORADIOLOGY 2014 -2015

Dra. Ramos Radiology

KIDNEYS
Minor calyces join to form major calyces (infundibula) which
1. Excretory urography (XU) or Intravenous pyelography (IVP) drain into the renal pelvis.
2. Ultrasound (US)
3. CT (MDCT) BLOOD SUPPLY
4. MRI
5. Contrast study: IVP or US  Laterally from the aorta,just below origin of the superior
mesenteric artery → main renal arteries originate
ANATOMY  Right renal artery courses posterior to the IVC
 Left renal artery courses posterior to the left renal vein.
Size of Adult kidney = 9-13cm (stable from ages 20-50, decreases
main renal artery
thereafter) ↓
Extends from T11-L3 ventral and dorsal branches as it enters the renal hilum
 After 50-60 years old magstop na sya mag grow ↓
Kidney is a retroperitoneal organ, it doesn’t communicate with divide into segmental arteries (supply separate portions of
any other borders of the intraperitoneal organs except with that the kidney)
of the pancreas  Each is an end artery without anastomoses.
 Surrounded by Gerota’s fascia (renal fascia) + perirenal fat  highly subject to infarction caused by
(renal shadow outline) (hypodense structure) emboli/occlusion.
 Perirenal fat shows stranding densities in cases of: ↓
1. inflammation Interlobar arteries (course in the columns of Bertin)
2. edema ↓
Arcuate arteries (course parallel the renal capsule at the
Peripheral cortex corticomedullary junction)
 immediately beneath the renal capsule ↓
Septal cortex Intralobular arteries.
 extends down between the pyramids as the columns of
Bertin.

Apex of each pyramid

 directed at the renal sinus
 projects into a calyx
 papilla → innermost zone of the medulla (closest to the
draining calyx)

Simple calyces
 cup-shaped structures that drain one renal lobe.

Compound calyces
 drain several renal lobes
 more common at the poles of the kidney
 more prone to intrarenal reflux.

Color Doppler US: demonstrate arterial divisions down to the

level of the arcuate artery

Renal sinus contains

 renal arteries,
 renal vein and
 some renal fat

Renal cortex contains

 glomeruli and
 proximal & distal collecting tubules

Renal medulla contains

 Long straight portions of loop of Henle
 collecting tubules

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 URORADIOLOGY 2014 -2015
Dra. Ramos Radiology
The calyces, pelvis, and ureter can only be demonstrated by the CT-IVP
use of Radioopaque compounds in IVP or Retrograde pyelography.  imaging method of choice in the evaluation of hematuria
 rapid thin-slice high-resolution scans
IMAGING TECHNIQUES  optimal evaluation of the renal parenchyma with
satisfactory assessment of the collecting systems, ureters,
XU/IVP and bladder
 Plain (pic) vs. Contrast (pic)  Cross sectional images only. It cannot do sagittal and
coronal sectional but MRI can. But MRI is too slow and too
costly.
 CT can form a reconstructed image. Lets say bibigyan ka ng
5mm thickess crossectional images, pagsasamasamahin yan
to form a coronal image.
 offers major advantage of markedly increased contrast
resolution compared to conventional radiography
 higher sensitivity for detection of
parenchymal renal lesions
 Precontrast scans
 to detect urinary stones
 calcifications
 provide a baseline to assess for the enhancement of
lesions
 Following intravenous contrast administration, arterial
phase scans through the kidneys show early enhancement
of renal tumors.
 Corticomedullary phase appearance
 renal cortex enhances before the renal medulla,
 medulla is unenhanced,
 small medullary lesions may be missed
during this phase.
st
 1 thing to light up (opacify) is the CORTEX because
it contains glomeruli
 if there is for example there is renal mass on the
cortex, hindi magtatakeup yun ng contrast. Meron
syang filling defect.

 Nephrogram phase
 Approximately 120 seconds following onset of
contrast injection
 renal parenchyma is normally uniformly
enhanced
 A pyelogram phase
 scan at 3 to 5 minutes
 contrast filling of the collecting system and
ureters.
 Contrast medium in a form of iodine is given IV usually in
the antecubital vein. MRI
 2mins. after bolus injection there is already nephropgraphic  When use of IV iodinated contrast is contraindicated
phase  CT study is equivocal
 Nephrogram ibig sabiihin renal parenchyma yung  Esp. in patients with if renal failure
tinitignan.  using contrast medium frequently can cause acute renal
 You can see already that the calyces and the urinary bladder tubular acidosis
are opacified. You can already see the left and right  MRI makes use of hydrogen ion, so it uses the urine, no
superior and inferior poles of the kidneys. need for the contrast medium
 Renal shadows: outlined by fat (radioluscent). Gerota’s  effective evaluation of uroepithelium even without IV
fascia encloses the renal compartment. Within Gerota’s contrast
fascia is your perirenal fat, so yung fat na yun is  best images when the ureters and collecting system are
radioluscent. Sabi natin pag fat mas maitim sya kesa sa soft dilated
tissue. Pag tinabi mo sya sa for example liver, mas maitim si
fat kesa kay liver. That is why on plain radiograph, this renal US
shadow, kahit wala pa syang contrast makikita mo parin ang  Screening tool for kidney size & hydronephrosis
renal shadow  Very fast, very cost effective.
 Doppler US
 Arcuate arteries: least diameter that can be seen

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 URORADIOLOGY 2014 -2015
Dra. Ramos Radiology

CONGENITAL ANOMALIES

I. Renal Agenesis

 Absent/underdeveloped
 Compensatory hypertrophy of the contralateral kidney
(>10% of N. renal volume)
 Incidental finding
 Radiologic Features:
 Absence of renal shadow
 Large kidney on other side
 Trigone deformed (absence of ureters and ureteral
orifice on the bladder are also absent)
 Angiography
 absence of renal arteries
 Delayed Nephrogram phase: Chronic Pyelonephritis
 hindi kagad magtatake up ng contrast yung diseased kidney,
so you wait for 1 hour and then lets see if wala talaga. Then
probably there is really agenesis.
 Look also for ectopic kidney using ultrasound. There are
times kasi na yung kidney, wala sya sa renal fossa.
Sometimes it is located lower or sometimes yung tinatawag
na pelvic kidney.

II. Horseshoe kidney

 MOST COMMON renal fusion anomaly

 Usually supplied by multiple arteries w/ ectopic origins
 lower poles of the kidneys are joined across the midline by
a fibrous or parenchymal band
 As a result of fusion, the kidneys are malrotated, with the
renal pelvises directed more anteriorly and the lower pole
calyces directed medially.
 The fused kidney is low in position in the abdomen
because normal ascent is prevented by the renal tissue
encountering the inferior mesenteric artery in the midline
 Complications: urinary stasis
 hydronephrosis, stones, infection
 Radiologic features:
 Alteration of the orientation. This time, the renal
hilum is directed anteromedially
 Lower pole should be directed laterally, but this time,
medially because of the isthmus
 Lower pole fused US
 isthmus prevents the normal ascent of the kidney

III. Crossed-fused renal ectopia

 May present as an abdominal mass (made native kidney

larger) because 2 kidneys are fused on the same side of
abdomen
 Kidney crossed the midline and fuse with the native kidney
on the other side
 It is ectopic because it is not in its native position
 Renal arteries – invariably aberrant
 Ureters insert in normal locations in bladder trigone
CONFIRMS the DIAGNOSIS
CT
US

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SOLID RENAL MASSES  Composed Varying amounts of smooth muscle, fat, and
abnormal blood vessels lacking elastic tissue
I. Renal Cell Carcinoma (RCC) (PATHOGNOMONIC)
 80% unilateral
 MOST COMMON  20% tuberous sclerosis (multicentric & bilateral)
 85% of all renal neoplasm  Prone to hemorrhage (massive) due to abnormal thin
 M:F – 3:1 –(HAHAHA!!!!-sabi ni doc lol) walled vessels
 50-70 yo  May be as large as 20cm, predominantly exophytic, mimic
 Unilateral (98%) nonrenal tumors
 MDCT: tumor evaluation & staging (method of choice)  MDCT: usual DIAGNOSTIC METHOD OF CHOICE
 Metastasize usually in the liver, lungs and bone  Fat density w/in a solid renal tumor without
 Radiologic features: calcification - DIAGNOSTIC
 Hemorrhage: contrast extravasation  Radiologic features:
 No collaterals  It should be a mass with FAT component but
 Necrosis (liquefaction)- will give you a complex WITHOUT CALCIFICATION
appearance, hypodense foci  Range from purely fat density to nearly
homogenously solid muscle density
 Fat & calcification: metastasis from bone marrow
 Hypodense structure – fat (below 0 Hu)
 Nodules– smooth muscle & vascular components
 Strands – soft tissue density
 Fat on US: hyperechoic

pointed: Foci of Hemorrhage & Necrosis

 Cystic/multicystic or solid – ultrasound

-pointed: (Cysitc RCC) distinct tumor nodule in the
perirenal fat is highly indicative of tumor extension
outside of the renal capsule

- Pointed: fat density w/mixed strands & foci of

soft-tissue density (characteristic of AML)

 Indistinguishable from RCC – needs biopsy

III. Oncocytoma

 Oncocytes: eosinophilic cells

 Rare (3-6%)
 Hemorrhage & necrosis rare
 Well encapsulated and benign
 Indistinguishable from RCC – needs biopsy
 Calcification (10%)- more seen in CT  CENTRAL STELLATE SCAR- suggestive of oncocytoma
 Hypervascular- meaning if you give contrast, it  these are radiating vascular structures from the
assumes the hyper opacification of the cortex middle
 Renal vein invasion (20-30%) & IVC (4-10%)
 Distant metastases
 Definitive Treatment: Resection
 Renal mass, is always diagnosed as RCC unless proven
otherwise because RCC has a wide spectrum of
appearances

II. Angiomyolipoma (AML)

 Uncommon (1-3%)
 Benign mesenchymal tumor

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 URORADIOLOGY 2014 -2015
Dra. Ramos Radiology
IV. Lymphoma CYSTIC RENAL MASSES

 Very rare I. Simple Renal cyst

 Usually metastastic or by direct invasion
 It enlarges the kidney, can be diffusely enlarged, can be  MOST COMMON Rema;,ass
focal or lobar enlargement, multiple bilateral solid renal  Fluid containing
masses, perirenal tumor surrounding the kidney  Asymptomatic when small (<4cm)
 Mostly non-Hodgkins  Large cysts (>4cm) can cause obstruction, flank pain,
 (+) extensive retroperitoneal adenopathy- diagnostic of hematuria, or hypertension
lymphoma  Usually multiple bilateral
 Hindi na nakikita yung aorta signifying  On XU: BEAK- DEFORMITY – “CLAW SIGN” – since you
lymphadenopathy have a cystic lesion, it will occupy the renal cortex, pag nag
 Poor delineation of corticomedullary junction opacify yung cortex, yung normal cortex lang mag
 “bulky tumor” oopacify, but the renal cyst will not opacify, because there
 There is also bulging within the retroperitoneum (tumor are no blood vessels within that cyst, there will be filling
invasion) defect. Renal cortex and renal parenchymal will be split
 CT: homogenous & poorly enhancing apart by the cyst, therefore showing the claw sign. (yung
 MR: isointense or slightly hypointense to renal paligid lang nung cyst yung nagoopacify kaya claw sign—
parenchyma matinding imagination please lol)

Arrowhead: impaired contrast enhancement of R.

kidney caused by lymphomatous involvement of R.
renal blood vessel.

V. Metastases

 Kidneys – frequent site of hematogenous metastases

(most detected late)
 Most appear as multiple, bilateral, small, irregular,
infiltrative renal masses
 Common primary tumors: lung, breast, melanoma, & colon
carcinoma
 Hypodense masses
- Typically infiltrative & poorly defined

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Dra. Ramos Radiology

 US – most cost effective imaging tool to diagnose cystic

kidney
1. Round or oval anechoic mass- wala syang echo sa
loob talagang fluid lang,
2. thin/imperceptible cyst wall
3. Increased posterior-through transmission -when an
organ is cystic or fluid filled it doesn’t show any
echoes but instead, shows enhancement posteriorly
4. Sharply defined far wall

 MR criteria
1. Homogenous, sharply defined round/oval mass
2. Homogenous low-signal intensity
3. Homogenous high-signal intensity
4. No enhancement after gandolinium administration

II. Complicated Renal cyst

 Simple renal cysts complicated by hemorrhage or infection

 Bosniak classification – to determine management of
lesions

Bosniak classification
 Category 1 - simple renal cyst – fluid density, no
nodularity, no septations. CT, MR, & US are definitive
when all characteristic findings are present
 Category 2 – benign, minimally complicated cyst;
increased attenuation values, thin calcifications, thin
septation
 US, CT, & MRI each make a definitive diagnosis  3 types of cysts
1. cysts w/ delicate thin septations not >1mm-
 Definitive CT signs 2mm thick,
1. Sharp margination w/ the renal parenchyma 2. cysts w/ delicate thin calcification in
2. No perceptible wall wall/septum,
3. Homogenous attenuation near water density (- 3. “high-density” cysts that are hyperdense (60-
10 to +10H) 100H) on CT bec. Of high concentration of
4. Absence of contrast enhancement protein or blood breakdown products and
 the cyst should be fluid like in density = 0 Hu =fluid. are <3cm in size
 pag (Hounsfield unit)Hu is more than 0, there could  Category 2F – likely benign but require additional follow-
be a necrotic debris, hemorrhage, Hu can be 40, 50, up imaging to confirm benignancy. Follow –up at 3, 6, & 12
etc. mos.
 if I see thin septations and calcification, its not type I  Thin septa/minimal smooth thickening of walls/septa
(simple Cyst) anymore. but without measurable contrast enhancement,
 thick or nodular calcification in wall (intrarenal
nonenhancing high-density cysts <3cm)

- Classified as Bosniak II. Pointed: small simple

renal cyst & a larger renal cyst complicated by
thin rim of calficiation
- CT features characteristic

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 Category 3 – indeterminate lesions (benign or malignant)  Classified as Bosniak III or IV
with thick irregular calcification, irregular margins, thick or  Middle aged-women (40-60)
enhancing septation or chunky calcifications, areas of  Surgical excision (indistinguishable from multicystic RCC)
nodularity, uniform thick wall and multilocular mass
 Multilocular cystic nephroma, multilocular clear cell RENAL CYSTIC DISEASE (that are not seen as masses)
RCC, complex benign hemorrhagic or chronically
infected cysts I. Autosomal Dominant Polycystic Kidney Disease (AD PKD)
 Category 4 - clearly malignant necrotic cystic neoplasms
that arise in the wall of a cyst  Manifests later in life
 Irreg. solid nodules, irreg. thick shaggy walls,  Renal parenchyma is progressively replaced by multiple
enhancing components, solid enhancing nodules, noncommunicating cysts of varying size
calcification present, and nodular septations  Are seen in children but are asymptomatic. They become
symptomatic by the age of 30-50yo with Hypertension
BOSNIAK CLASSIFICATION and Renal failure
 Type 1 = no chance of malignancy  Greatly enlarged kidneys (increased renal volume)
 Type 2 = may have chance of malignancy  Complicated by internal hemorrhage
 Type 3 = 57% probability of malignancy  Liver cysts (60%)
 Type 4 = 100% malignant  Pancreas cyst (10%)
 Cardiovascular abnormalities : intracranial aneurysms
III. Renal abscesses (20%), mitral valve prolapse, bicuspid aortic valve, aortic
aneurysms & dissection
 Usually results from pyelonephritis complicated by  US- Multiple varisized*(please check spelling haha) cyst,
liquefactive necrosis non communicating. In comparison with miltilocural cystic
 Most common appearance: focal renal mass w/ thick wall nephroma, it is seen as a mass, but here, kindey is
 Inflammatory changes: stranding densities in perirenal transformed into a cystic mass itself.
space & thickening of renal fascia  CT – innumerable cysts w/ varying attenuation of internal
fluid (episodes of hemorrhage & infection)

- Thick wall & septations & internal fluid density.

Edema is present (reduces CT density)

 May extend into perirenal space – perirenal fluid collection II. Autosomal Recessive Polycystic Kidney Disease (AR PKD)
 air pockets w/in mass –compare air within the bowel
 US: complex mass- it can be interpreted as RCC but if you
have prior history of pyelonephritis then most probably, it
is renal abscess.
st
 1 differential: RCC can be cystic, so do not ignore

IV. Multilocular Cystic Nephroma

 Adult cystic nephroma or mixed epithelial and stromal

tumor (MEST)
 Uncommon benign consisting of non-communicating cysts
of varying size separated by connective tissue septations
 Neonates, children, detectable in fetus
of varying thickness
 Primary defect: fusiform dilatation and lengthening of the
 Because if they are communicating, they are not cyst
collecting tubules
anymore, they are dilations of the calyces, it is
 Throughout renal parenchyma
hydronephrosis.
 Bilateral, symmetrically & markedly enlarged

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 More hyperechoic than AD PKD kasi maliliit lang yung cyst
nila.. mas tabi tabi sila.
 Usually they have no extra renal cyst but they have
hepatic fibrosis so they develop portal HPN
 US – used to make diagnosis
 both kidneys large and echogenic centrally with a
sonolucent rim of compressed cortex
 Visualized cysts <5 mm
 enlarged echogenic liver, cystic dilatation of
intrahepatic bile ducts, splenomegaly, dilated
portal vein, and enlarged portosystemic collateral
vessels.

III. von Hippel-Lindau disease

 multiple renal cysts (60%), multiple bilateral RCC (24-45%),

adrenal pheochromocytoma, pancreatic cysts (serous
cystadenoma), & pancreatic adenocarcinomas  US: hyperechogenic medulla renal pyramids are also
 Autosomal Dominant hyperechogenic (image below)
 Retinal angiomas, cerebellar hemangioblastomas,
pheochromocytoma and pancreatic cyst
 Multiple simple renal cysts; 1/3 RCC
 More likely of renal angiolipoma

IV. Acquired Uremic Cystic Kidney Disease

 Develop multiple cysts in native kidneys in long-term

dialysis patients
 Incidence 90% - 5-10yrs of hemodialysis
 small kidneys less than 9cm (chronic renal dse)
 cyst (predominantly cortical) are multiple and less than
2cm in size
 eventually they develop retro peritoneal hemorrhage and
RCC (7%).
VI. Uremic Medullary Cystic Disease

 Presents w/ renal failure, anemia & salt wasting

 Basic defect: progressive tubular atrophy w/ glomerular
sclerosis & medullary cyst formation
 Renal parenchymal echogenicity is usually increased

VII. Multicystic Dysplastic Kidney

 Ususally diagnosed in utero or at birth

 Only 1 kidney as mass of non-communicating cyts with
- Both kidneys small & contain numerous small usually absent or atretic ureter.
cysts (hemodialysis px for 8 yrs) o It is non functional, will eventually atrophy and then
calcified, so its just the same with your renal agenesis
V. Medullary Sponge Kindey

 Non cystic but looks cystic on imaging

 Dysplastic dilatation of collecting tubules in the papilla
 Dilation is cylindrical/saccular
 Urinary stasis >> stone form
 Causes urinary stasis kasi dilated. Less transport of urine
from the pelivis. If you have stasis- infectionstone
 Most are asymptomatic
 No genetic predisposition & No risk of renal failure
 CT or MR: most characteristic
 papillary striation & saccular contrast collections
 since dilated sila, after madrain nung contrast,
may natitira parin sa dilated portions ng kidney

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- CT angiogram: tangle of large vessels & enlarged arteries and

veins.

RENAL INFECTION

I. Acute Pyelonephritis

 Usually result of ascending UTI

 Caused by Gm (-) organisms, especially E. coli
 Predisposing factors: diabetes, obstruction, immune
system compromise, drug abuse, chronic debilitating
disease, and incomplete antibiotic treatment.
 Normal imaging in UNcomplicated cases
 CT more sensitive than US in showing subtle
changes in uncomplicated pyelonephritis
 Complicated: renal/perirenal abscess
 CT or US
RENAL VASCULAR DISEASES
 Striated nephrogram: hypodense foci within the renal
cortex (edema, inflammation)
I. Renal arteriovenous malformations (AVM) & arteriovenous
 streaks and wedges of low attenuation extending
fistula (AVF)
to the renal capsule associated with thickened
septa in perinephric fat and thickening of Gerota
 Congenital (25%) or cirsoid AVM
fascia. (definition in the book)
 Nest of torturous vessels just beneath the
 MR – enlargement due to edema & hemorrhage &
uroepithelium
perinephric fluid collections
 Frequently cause hematuria
 CT – obstructing calculi & gas well demonstrated
 Acquired(75%)
 Complications: intrarenal or perirenal abscess
 Fistulous connections between intrarenal arteries
& veins
 Caused by renal biopsy, trauma, surgery, or
malignant tumors
 Radiologic features:
 CT w/o contrast – blood in collecting sys. & cortical
atrophy
 Postcontrast CT – filling of a network of vascular
structures (renal v. dilated if shunt is large)
 Doppler US – nest of vessels w/ mixed color,
turbulence, & tissue vibration artifact
 MR Angiography – less sensitive for slow-flow
lesions but shows feeding & draining of high-flow
lesions

- Edema and swelling; arrowhead shows wedge-shaped

defects

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II. Emphysematous Pyelonephritis

 Hyopdense
 Form of acute pyelonephritis with air in renal
parenchyma (–) 1000 Hu
 Occur in patients w/ diabetes, obstruction, or immune
compromise
 Rapidly progressive, often life threatening
 Mixed flora inf. w/ Gm (-) organisms most common
 Acute, enlarged
 Plain radiograph & CT
 streaks and collections of gas within the renal
parenchyma

-
deep cortical scar overlies a blunted calyx
(arrow)
V. Xanthogranulomatous pyelonephritis

 rare destructive granulomatous process may diffusely

involve an obstructed kidney or present as focal renal
mass
 chronically infected, most commonly Proteus mirabilis
 Renal parenchyma destroyed → replaced by xanthoma
cells (lipid-laden macrophages)
 CT and US
 focal or diffuse hydronephrosis and a complex
mass with areas of high and low density.
 Inflammatory changes extend into perinephric fat
 MR
 dilated calyces compressing and intrarenal
abscesses replacing renal parenchyma.
- striations in renal parenchyma caused by
interstitial gas

 US: dirty acoustic shadowing- air

III. Emphysematous Pyelitis

 Infection with gas confined to renal collecting system,

sparing the parenchyma
 Less aggressive, morbidity is not as high

IV. Chronic Pyelonephritis & Reflux nephropathy

 chronic interstitial nephritis caused by infection

 MOST COMMON Cause
 Calculi and chronic obstruction: adults
 Veiscoureteral Reflux of infected urine: children
 Reflux nephropathy - progressive renal injury associated - large obstructing stone (black arrow) occupying the
with reflux renal pelvis. Calyces (arrowhead) are dilated and the
 Intrarenal reflux - most prominent at the upper pole parenchyma is atrophic and replaced by inflammatory
within compound calyces→damages the papilla, → tissue. Indolent abscess (white arrows)
calyceal blunting with overlying cortical scarring
 Predisposing conditions: neurogenic bladder, ileal
conduits, & other causes of urinary stasis
 XU/CT: Focal cortical scarring overlies blunted calyx
(HALLMARK) – normal calyces, there should be cupping
(cup like)
 Classically lobar - Interposed normal tissue (alternating
normal and scarred tissue)

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VI. Renal Tuberculosis Kindeys are chronically diseased
CT IVP - Usually kidneys are not functioning, they do not take up
 Just like in the lungs it cause parenchymal destruction the dye so di mo na sya makikita
 Usually follow primary pulmpnary TB by 10-15yrs before it
shows I. Renal Failure
 Active pulmonary TB (10%)
 Urinary tract is the most frequent site of extrapulmonary  US requested:
tuberculosis  to exclude hydronephrosis,
 Presentation: asymptomatic hematuria or sterile pyuria  assess renal size,
 identify renal parenchymal disease
 HALLMARKS:  often require biopsy for definitive diagnosis of renal
 papillary necrosis, parenchymal disease.
 parenchymal destruction,  small (<9 cm) kidneys - irreversible end-stage renal disease
 cavity formation → uneven calyectasis, and do not benefit from biopsy.
 fibrosis and scarring of the collecting system and  Measurements of renal cortical thickness - unreliable in
the renal parenchyma, assessing residual renal function.
 parenchymal masses owing to granuloma  Sonographic signs of renal parenchymal disease
formation,  diffuse increase in parenchymal echogenicity
 strictures of the collecting system and ureters, associated with loss of corticomedullary
 widely variant patterns of calcification (40% -70%) differentiation
 Alteration in kidney size
 End-stage nonfunctional tuberculous kidneys II. HIV-associated renal disease
 Appear as hydronephrotic sacs or atrophic and
calcified masses in the renal bed  Include HIV nephropathy, opportunistic infections,
 “putty kidney” – caseous necrosis w/ calcification lymphoma, Kaposi sarcoma, and renal disease secondary
(image below) to antiretroviral therapy
 HIV nephropathy is the primary cause of renal failure
 US findings:
 normal or enlarged
 highly echogenic kidneys - renal failure
 CT findings:
 enlarged kidney with high-attenuation medullary
regions on noncontrast scans
 striated nephrogram on postcontrast scans
 MR findings:
 renal enlargement and loss of corticomedullary
differentiation.

RENAL PARENCHYMAL DISEASE

diffuse hyperechogenicity – you cannot see the corticomedullary

junction

 Opportunistic infections: Pneumocystis carinii, P. jiroveci,

Mycobacterium avium intracellulare, M. tuberculosis,
Candida albican, and Aspergillus.
 Kaposi sarcoma - renal enlargement with irregular cortical
low-attenuation areas on CT.
 Antiretroviral theray (indinavir)
 unusual calculi: cause obstruction, hydronephrosis,
and pain.
 Indinavir-induced crystals precipitate in the tubules
and cause defects in enhancement in the renal
parenchyma and parenchymal atrophy.

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NEPHROCALCINOSIS  US
 imaging method of choice for screening
pathologic deposition of calcium in the renal parenchyma hydronephrosis
usually bilateral and the result of systemic disorders  limited ability in small uroepithelial tumors

I. Cortical Anatomy
 Unusual (<5%)  Collecting tubules of a medullary pyramid coalesce into the
 acute cortical necrosis, chronic glomerulonephritis, severe papillary ducts that pierce the tip of the papilla and drain
ischemia, primary hyperoxaluria into the receptacle of the collecting system called a minor
calyx.
II. Medullary  The projection of a papilla into the calyx produces a cup
 More common shape.
 Related to hypercalcemia or hypercalciuric states  The sharp-edged portion of the minor calyx projecting
 Echogenic renal pyramids around the sides of a papilla is called the fornix of the calyx.
 Urate deposition can also be the cause  Compound calyces found at the poles of the kidney formed
by the projection of two or more papilla into the calyx.
CAUSES OF MEDULLARY NEPHROCALCINOSIS  Infundibula extend between minor calyces and the renal
pelvis.
 The renal pelvis is triangular, with its base within the renal
sinus. The apex of the pelvis extends outward and
downward to join the ureter.
 A so-called extrarenal pelvis is predominantly outside the
renal sinus
 larger and more distensible than the more common
intrarenal pelvis, surrounded by renal sinus fat and
other structures
 normal variant that should not be confused with
hydronephrosis
 The ureters have an outer fibrous adventitia that is
continuous with the renal capsule and the adventitia of the
bladder.
 The muscularis (outer circular and inner longitudinal muscle
bundles) for ureteral peristalsis.
 Mucosa lining the entire pelvicalyceal system, ureters, and
bladder is transitional epithelium.
 The ureters enter the bladder at an oblique angle. When the
bladder wall contracts, the ureteral orifices are closed. The
ureters propel urine by active peristalsis, which can be
visualized fluoroscopically and by US.
 Jets of urine opacified by contrast are frequently seen
- Patient w/ medullary sponge kidney: calcifications in medullary within the bladder on CT.
region, stones form in dilated collecting tubules in medullary pyramid

COLLECTING SYTEM (Pelvicaliceal system)

minor calyx, major calyx, pelvis, ureters, urinary bladder

Evaluation
 CT IVP
 imaging method of choice for hematuria
 screening examination
 MRI
 Retrograde pyelography
 cystoscopic catheterization of the ureteral orifice
followed by injection of contrast
 independent of renal function 3 mainpoints of Ureteral Narrowing (where calculi are likely to be
 provides high-quality images of the ureter and the impacted)
collecting system, 1. Ureteropelvic junction (UPJ)
 another alternative commonly utilized by urologists 2. Ureterovesical junction (UVJ)
 Antegrade pyelography 3. Site at which ureter crosses the pelvic brim/iliac arteries
 When a percutaneous nephrostomy catheter is
present

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CONGENITAL ANOMALIES

I. Ureteral Duplication

II. Bifid renal pelvis

 one ureter, 2 renal pelvis

 Separate pelvises draining the upper and lower poles join
at the UPJ
 10% of population
 No pathologic consequences

III. UPJ obstruction

 May go undiagnosed until adulthood

 Ureter should be normal, but proximal to that (pelvis and
calices) are dilated. Usually are secondary to an
embryologic constriction. Results from patent but
aperistaltic ureter
 US
 pelvicalyectasis with sharply defined narrowing at
the UPJ. The ureter is not dilated.
 1-2% of population  15-20% aberrant renal vessel causes the obstruction
 Unilateral 6x more common than bilateral
 Duplex Ureter : Weigert-Meyer Rule IV. Retrocaval ureter
 with complete ureteral duplication, the ureter
draining the upper pole passes through the bladder  posterior to IVC (dapat kasi anterior sya)
wall to insert inferior and medial to the normally  developmental variant - right ureter passes behind the IVC
placed ureter draining the lower pole. at the level of L3 or L4
 Upper pole moiety: medial & inf. to ureter  The ureter exits anteriorly between the cava and the aorta
insertion (ectopic) and ends as a ureterocoele – to return to its normal position.
prone to obstruction  urinary stasis and proximal pyeloureterectasis.
 Lower pole moiety: at/near normal insertion in the  Faulty embryogenesis of the IVC, with abnormal
urinary bladder - prone to vesicoureteral reflux persistence of the right subcardinal vein anterior to the
 Females: ectopic ureter may insert into the lower bladder, ureter instead of the right supracardinal vein posterior to
upper vagina, or urethra the ureter.
 Males: insert to lower bladder, prostatic urethra, seminal  proximal ureter as well as the pelvis and calyces are
vesicles, vas deferens, or ejaculatory duct. dilated because the rest of the ureter is behind the IVC
 Drooping lily appearance: lower pole moiety displaced
inferiorly – because it is hydronephrotic
 Upper pole system
 Cystic dilatation with marked parenchymal thinning
 tortuous and dilated.
 Ectopic ureterocele & associated dilated ureter →
multiseptated cystic mass in the pelvis

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RENAL STONE DISEASE Classic appearance of ureterolithiasis

noncontrast CT – diagnosis of acute ureteral obstruction by renal  high-attenuation stone within the ureter associated with
stones (97% sensitivity, 96% specificity) proximal dilatation and distal contraction of the ureter
Nephrolithiaisis  Findings of ureteral obstruction
 presence of calculi in the renal collecting system 1. mild dilatation of the pelvicalyceal system and ureter
Scout film: calcific density (>3 mm) proximal to the stone,
2. slight decrease in attenuation of the affected kidney
 Calcium phosphate & Oxalate – 80% (MOST COMMON) caused by edema
 radiopaque 3. perinephric soft tissue stranding representing edema in
 Brushite – 2-4% the perinephric and periureteral fat.
 Unique form of clcium phosphate; tend to recur
quickly if not treated aggressively  Tissue rim sign
 Resistant to Tx w/ shock wave lithotropsy  halo of soft tissue surrounding the calculus
 Struvite (Magnesium ammonium phosphate) – 5-15%  Phlebolith (-)
 Formed in presence of alkaline urine & infection  calcification within thrombosed veins
 Radiopaque commonly in the pelvis
 Most common component of staghorn calculi  tissue rim sign is absent
 Tail sign: tubular tail extending from the
calcification representing a thrombosed
vein

 Ureteric stone
 ureteric inflammation surrounding it
 (+) tissue rim sign
- Staghorn calculi

 Cystine stones – 1-2%

 Mildly radiopaque
 Px w/ congenital cystinuria
 Uric acid & Xanthine – 5-10%
 radioluscent – CT lang sya makikita

CT Stonogram: w/o contrast → presence of stone

Stones <6mm – pass spontaneously w/in 6 wks
Stones >6mm – likely to remain lodged & require removal
Calculi usually lodges at the three areas of narrowing

HYDRONEPHROSIS

Renal calculi complication

Dilatation of the upper urinary tract w/potential progressive
 urinary obstruction, ureteral stricture, chronic renal
destruction of renal parenchyma
infection, loss of renal function.
Calyctasis- dilation of the calyces
 Acute flank pain - common complaint
Pelvictasia- dilation of pelvis
 Renal colic - calculus obstructing the ureter
Pelvocalictasia- dilation of whole structure
 most common cause of acute flank pain and
Ureterectasis – ureteral dilatation
is the usual major consideration for
diagnostic imaging

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III. Pyonephrosis
 infection in an obstructed kidney
 rapid destruction – treated promptly by ureteral stent or
nephrostomy tube
 US
 Dilated collecting system filled w/ layering
echogenic pus & debris
 Shadowing calculi
 CT – better demonstration of site & cause of obstruction
 thickening (>2 mm) of the wall
 urine of higher than normal attenuation →
presence of pus.

IV. Veriscoureteral reflux

 common cause of hydronephrosis in children

I. Peripelvic cysts  abnormal ureteral tunnel at the UVJ and associated UTI
allowing infected urine from the bladder to reflux up the
 multiple or multilobulated cysts that occupy the renal ureter.
sinus.  Adults - neurogenic bladder or bladder outlet obstruction.
 contain clear fluid and may be lymphatic or posttraumatic  confirmed by demonstrating retrograde filling of the
in origin. ureters on voiding cystourethrography or radionuclide
 mimic hydronephrosis on noncontrast CT, MR, & US cystography.

II. Obstructive uropathy - but you can also have non obstructive V. Congenital megaureter

 Causes of Obstruction – tumors, renal calculi, strictures  aperistaltic segment of the lower ureter 5 to 40 mm in
secondary to radiation therapy, and compression length → functional obstruction → dilatation of the
 more proximal and the more chronic the obstruction, the proximal ureter
greater is the degree of dilatation  Ureteral dilatation exceeds 7 mm.
 US  The aperistaltic segment of the ureter - smoothly tapered
 separation of normal sinus echogenicity by narrowing without evidence of mechanical obstruction.
anechoic urine in the collecting system
 calyces enlarged and blunted and are seen to VI. Prune belly syndrome (Eagle–Barrett syndrome)
connect with the dilated renal pelvis
 Hypoechoic medullary pyramids – children  congenital disorder - absence of the abdominal wall
 Pyramids more peripheral, surrounded by more musculature, urinary tract anomalies, and cryptorchidism
echogenic cortex, do not connect with the renal  Mostly males
pelvis.  ureters are markedly dilated and tortuous, bladder is large
 MDCT signs of obstruction and distended, posterior urethra is dilated
 increasingly dense nephrogram with time,
 delay in appearance of contrast in the collecting
VII. Polyuria
system,
 dilated pelvicalyceal system and ureter to the
point of obstruction.  Acute diuresis & diabetes insipidus
 Mild to sever hydronephrosis

MASS or FILLING DEFECTS

I. Calculi – MOST COMMON

 >85% radiopaque
 CT density >200H
 MR – foci of absent signal w/in the collecting system

- medulla & collecting system is NOT enhanced II. Blood clots

 Non-obstructive hyrdronephrosis  Nonradiopaque

o Causes – diabetes insipidus, over hydration, UTI, intra-  CT attenuation values: 40-80H
abdominal inflammatory disease

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III. Transitional Cell Carcinoma (TCC)  Slough papilla – cause obstruction and colic

 85-90% of uroepithelial tumors - filling with contrast at lower poles

nd
 2 MOST COMMON PRIMARY RENAL MALIGNANCY (10%) VII. Fibroepithelial polyp
 85% Papillary growth pattern (exophytic, polypoid,
attached to mucosa by stalk)  benign fibrous polyp covered by transitional epithelium.
 Characteristic stippled pattern of contrast material  Common in yound adult men
within the interstices  seen as column of filling defect
 Secondary to chemicals (textile & plastic), drugs
(cyclophosphamide&phenacetin), smoking, and chronic VIII. Pyelourethritis cystica
urinary stasis (horseshoe kidney)
 metastasizes most commonly to regional lymph nodes,
liver, lung, and bone  Submucosal cysts formation assoc. w/ chronic UTI
 Retrograde pyelography/Excretory Urography  Uereter has multiple cyst, so pag cyst sya di pupunta dun
 “amputated calyx” – completely obstructed tumor yung contrast.
will not fill with retrograde-contrast  Multiple, small (2 to 3 mm), smooth, round filling defects
 “apple core lesions” in the ureter in the ureter (CHARACTERISTIC)
 Champagne glass sign – ureteral dilatation distal to  Cysts in renal pelvis are larger (2cm)
a filling defect. contrast trickled around the
obstruction and will continue to flow to the distal IX. Leukoplakia
ureter
 This sign distinguishes tumor from a  Rare, due to chronic UTI & calculi
calculus that impacts in the ureter and  Squamous metaplasia with keratinization & desquamation
causes distal spasm and narrowing. → irregular plaques in the renal pelvis, proximal ureter,
and bladder.
 key clinical feature - passage of flakes of desquamated
epithelium in the urine.
 premalignant condition in the bladder, but not in the
ureter.

X. Malakoplakia

 Also rare, inflammatory granulomatous condition of the

uroepithelium associated with chronic infection, especially
IV. Squamous Cell Carcinoma (SCC) due to Escherichia coli
 Smooth submucosal nodules composed of histiocytes
 10% uroepithelial tumors produce multiple smooth nodules in the distal ureter and
 Secondary to chronic infection, calculi, & phenacetin abuse the bladder.
 Imaging appearance indistinguishable from TCC  Not premalignant but can be aggressive extending outside
of the urinary system.
V. Metastases

 Common primary tumor sites are breast, melanoma, STRICTURES

cervix, lung and stomach
1. Inflammation from stone
VI. Papillary necrosis 2. Postraumatic
3. Uroepithelial tumor
 ischemic necrosis of the tips of the medullary pyramids 4. TB & Schistosomiasis
 secondary to infection, tuberculosis, sickle cell disease, 5. Extrinsic encasement by tumor/inflammatory processes
diabetes, and analgesic nephropathy.
 May remain in situ – mobile filling defect
PAPILLARY CAVITIES

 Calyceal diverticuli
 Uroepithelium-lined cavities that communicate
through a narrow channel with the fornix of a
nearby calyx
 Papillary Necrosis
 Cavities at the papillary tips that fill w/ contrast on
both antegrade and retrograde studies

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URINARY BLADDER  Urachal Carcinoma – ususally adenocarcinoma (90%)

ANATOMY
 The normal filled urinary bladder is oval, floor parallel to, and 5 - THICKENED BLADDER WALL/SMALL BLADDER CAPACITY
10 mm above, the superior aspect of the symphysis pubis
 Superior surface by peritoneum, which extends to the side walls I. Benign Prostatic Hypertrophy (BPH)
of the pelvis.
 The sigmoid colon and loops of small bowel, as well as the uterus  50-70% men older than 50
in females, lie on top of the bladder and may cause mass  Prostate enlargement projects into base of bladder,
impressions on the bladder dome. uplifting bladder trigone, and cause J-hooking of the distal
 The inferior surface is EXtraperitoneal. Anteriorly, the bladder is ureters
separated from the symphysis pubis by fat in the extraperitoneal  “J-hooking” – small bladder capacity. Why? Due to the
space of Retzius. enlarged prostate gland. The prostate gland compresses
 Posteriorly, the bladder is separated from the uterus by the the floor to the urinary bladder, uplifted yung trigone, so
uterovesical peritoneal recess in females and from the rectum magfoform syang jhooking sign
by the rectovesical peritoneal recess in males.
 The lining mucosa of the bladder is loosely attached to the
muscular coat, and therefore when the bladder is contracted,
the mucosa appears wrinkled.
 The bladder wall has 4 layers: an outer connective tissue
adventitia, smooth muscle consisting of circular muscle fibers
sandwiched between inner and outer layers of longitudinal
fibers, submucosal connective tissue (the lamina propria), and
the mucosa of transitional epithelium.
 The trigone is a triangle at the bladder floor formed by the two
ureteral orifices and the internal urethral orifice. With voiding,
the trigone descends 1 to 2 cm and transforms from a flat
surface into a cone with the urethra at the apex.

ANOMALIES
II. Urethral Stricture & Posterior urethral valves
I. Bladder Extrophy
 Chronic obstruction to outflow of urine
 congenital deficiency in development of the lower anterior  Bladder wall thickens in attempt to overcome obstruction
abdominal wall.  Shown by voiding/retrograde urethrography
 absent wall, bladder is open, mucosa is continuous with the
skin. III. Neurogenic Bladder
 Assoc. w/ Epispadias and wide diastasis of the symphysis
pubis  Spastic/atonic
 Ureteral obstruction, umbilical, and inguinal hernias are  Caused by meningomyelocele, spinal trauma, diabetes
common mellitus, poliomyelitis, CNS tumor, and multiple sclerosis.
 prone to urinary stasis, chronic infection, and stone
II. Urachal remnant diseases formation.
 eventually become trabeculated, thick-walled, and
 Asymtptomatic reduced in capacity
 Urachus - vestigial remnant of the urogenital sinus and
the allantois.
 tubular structure that extends from the bladder
dome to the umbilicus along the anterior
abdominal wall.
 The median umbilical ligament is its obliterated
residual
 Patent urachus (50%) - persistent communication between
the bladder and the umbilicus → urine leak
 Umbilical-urachal sinus (15%) – blind-ended dilatation of
urachus at umbilical end → persistent umbilical discharge
 Vesical-urachal diverticulum (5%) – outpouching of
bladder in ant. midline location of urachus → bladder
outlet obstruction as fluid-filled sac
 Urachal cyst (30%) – if urachus is closed at both ends but
patent in the middle

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CYSTITIS  TB – patchy calcification
 Cystitis – postirradiation, chronic inf., cyclophosphamide-
induced
inflammation of the urinary bladder wall. You see the radioluscency  Curvilinear or flocculent bladder wall calcification
around the urinary bladder.  Neoplasm – TCC & SCC (1-7%)
Many causes: infection (bacteria, adenovirus, TB, &
schistosomiasis), Drugs (cyclophosphamide), radiation, &
autoimmunity BLADDER WALL MASS or FILLING DEFECT
CT: bladder wall thickening & perivesical edema
MR: mucosal edema & inflammation I. Simple Ureterocoele

 cystic dilatation of the intravesicular segment of the ureter

caused by a congenital prolapse of the distal ureter into
the bladder lumen at the normal insertion site of the
ureter into the trigone
 incidental
 “cobra head” or “spring onion” appearance
 Radiolucent halo prodiced by wall of ureter outlined by
both inside & outside by contrast
 MRI: demonstrates pelvic sidewall destruction

I. Cystitis cystica – multiple fluid-filled submucosal cysts

II. Cystitis glandularis – further progression of cystitis cystica w/
proliferation of secreting glands in the lamina propria
III. Bullous edema – chronic irritation from indwelling chatheters.
Grape-like cysts elevate the mucosa
IV. Interstitial cystitis – chronic, idiopathic, most often women II. Ectopic Ureterocoele
V. Hemorrhagic cystitis – bacterial / adenovirus inf.
VI. Eosinophilic cystitis – unknown cause  Ususally assoc. w/ ureteral duplication
VII. Emphysematous cystitis – gas w/in bladder wall, assoc. w/ DM,  Females: prone to urinary incontinence
bladder outlet obstruction, E.coli infection  Ureter may insert to external sphincter into the
vestibule, uterus, or vagina
CALCIFIED BLADDER WALL  Males: usually insert proximal to external sphincter; no
incontinence results
If you see the bladder in plain radiograph, you have calcified
bladder wall usually seen on III. Vesical calculi

 Schistosomiasis – Schistosoma hematobium  May migrate from kidney or form primarily w/in bladder
due to urinary stasis or foreign body
  Solitary stones MOST COMMON
 Chronic bladder stones increases risk of developing
 bladder carcinoma
 echo & shadow

- noncontrast CT

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BLADDER WALL OUTPOUCHINGS & FISTULAS the bulbous urethra extending from the urogenital
diaphragm to the penoscrotal junction and the penile
I. Bladder Diverticula urethra extending to the urethral meatus.
 The anterior urethra is entirely contained within the corpus
spongiosum penis except for the proximal 2 cm of the
 herniations of the bladder mucosa between interlacing
bulbous urethra, called the pars nuda. This unprotected
muscle bundles
portion of the urethra is particularly susceptible to straddle
 Most are located posterolaterally near the UVJ
injury.
 The prostatic urethra runs vertically through the prostate
over a length of 3 to 4 cm. An oval filling defect in the
midportion of the posterior wall is the verumontanum. The
ejaculatory ducts open into the urethra on either side of the
verumontanum, and the prostatic glands empty into the
urethra by multiple small openings that surround the
verumontanum. The utricle, a mullerian remnant, is a small,
saccular depression in the middle of the verumontanum.
The distal end of the verumontanum marks the beginning of
the membranous urethra, which extends to the apex of the
cone of the bulbous urethra.
 The voluntary external urethral sphincter within the
urogenital diaphragm entirely surrounds the membranous
urethra.
II. Vesicocolonic Fistula  Cowper glands are pea-sized accessory sex glands within
the urogenital diaphragm on either side of the membranous
 most commonly occurs as a complication of diverticulitis urethra. Their ducts empty into the bulbous urethra 2 cm
 complain of pneumaturia and fecaluria. distally
 On retrograde urethrography, the bulbous urethra tapers to
III. Vesicovaginal fistula a cone shape as the urethra enters the external cone marks
the division between the membranous and bulbous
urethra. The penoscrotal junction that divides the bulbous
 usually complication of gynecologic surgery, especially for and penile urethra is marked by the suspensory ligament of
cervical carcinoma the penis, which causes a normal bend in the urethra.
 The entire anterior urethra is lined by the glands of Littre
IV. Vesicoenteric fistula whose secretions lubricate the urethra. Cowper ducts and
the utricle occasionally fill with contrast during
 almost always attributable to Crohn disease urethrography in a normal patient. The filling of these
structures with contrast occurs much more commonly in
URETHRA the presence of urethral strictures.
 Visualization of the glands of Littre is always abnormal and
Visualized thru Retrograde & Voiding urethrography associated with chronic inflammation and urethral stricture.
 Contrast medium is injected into the anterior urethra by Reflux of contrast into the prostatic ducts is also abnormal
means of a syringe or catheter that occludes the meatal and is associated with prostatitis and distal urethral
orifice. stricture.
 demonstrates distension of both the posterior and the  The female urethra varies in length from 2.5 to 4 cm. The
anterior urethra urethra is embedded in the anterior wall of the vagina and
 Can be also done in patients will renal insufficiency, hindi is lined throughout by periurethral glands.
ka pwede mag bigay ng IV contrast, so retrograde nalang

Voiding cystorethrougraphy (VCUG) or voiding urography

 performed by filling the bladder with contrast through a
catheter.

Anatomy
 The male urethra is divided into posterior and anterior
portions by the inferior aspect of the urogenital diaphragm
 The posterior urethra consists of the prostatic urethra
within the prostate gland, from the bladder neck to
urogenital diaphragm, and the short membranous urethra,
which is totally contained within the 1-cm-thick urogenital
diaphragm.
 The anterior urethra extends from the urogenital
diaphragm to the external urethral meatus. It consists of

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URETHRAL STRICTURES

 abnormal narrowings of urethra resulting from fibrous scar

tissue
 Most inflammatory attributable to gonorrhea
 Complications
 Periurethral abscess
 False passage (MOST COMMON) - iatrogenic due to
attempted passage of catheters
 Stasis & Infection
 Carcinoma of the urethra

POSTERIOR URETHRAL VALVES

 Usually discovered on prenatal US

 A thick valve-like membrane extends obliquely across the
urethral lumen from the verumontanum to the distal
prostatic urethra obstructing the flow of urine.
 Bladder outlet obstruction, bladder wall hypertrophy, &
bilateral hydronephrosis

URETHRAL DIVERTICULI

 smooth, sac-like outpouchings of the urethra

 congenital, infection, or trauma
 urinary stasis → stone formation & recurrent infection
(common complications)

TRAUMATIC INJURY

 10% pelvic fractures

 MOST COMMON SITE: junction between the prostatic and
the membranous urethra
 “straddle injury” - falling astride a fixed object : commonly
injures bulbous urethra.
 Complications: stricture, incontinence, impotence,
perineal sinus tracts & fistulas

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