GU Flashcards
Fetal lobulation
he fetal kidneys are subdivided into lobes that are separated with grooves. Sometimes this lobulation persists into adult life.
Fetal Lobulation VS Scarring:
Lobulation = Renal surface indentations overlie the space between the pyramids
Scarring = Renal surface indentations overlie the medullary pyraminds
Dromedary Hump
Focal bulge on the left kidney, which forms as the result of adaptation to the adjacent spleen.
Renal Agenesis
overview
- Congenital absence of one or both kidneys. If it’s unilateral this can be asymptomatic. If it’s bilateral think about the “Potter Sequence.” When it’s unilateral (it’s usually sporadic), for the purpose of multiple choice think about associated GYN anomalies in women (70% of women with unilateral renal agenesis have associated genital anomalies - unicornuate uterus). With regard to men, 20% with renal agenesis have absence of the ipsilateral epididymis and vas deferens or have an ipsilateral seminal vesicle cyst.
Renal Agenesis
associations
Ipsilateral seminal vesicle cysts, absent ipsilateral ureter, absent ipsilateral hemitrigone and absent ipsilateral vas deferens.
Potter Sequence:
Insult (maybe ACE inhibitors) = kidneys don’t form, if kidneys don’t form you can’t make piss, if you can’t make piss you can’t develop lungs (pulmonary hypoplasia).
Mayer-Rokitansky-Kuster-Hauser:
Mullerian duct anomalies including absence or atresia of the uterus. Associated with unilateral renal agenesis.
Lying Down Adrenal or “Pancake Adrenal” Sign
describes the elongated appearance of the adrenal not normally molded by the adjacent kidney. It can be used to differentiate surgically absent vs congenitally absent.
Corticomedullary Phase (CMP)
angio nephrographic - i f you
wanna sound like a pretentious prick
25- 40 Seconds
Contrast in the vascular system and the extracellular interstitial space
Cortex is enhanced the medulla is not (hence the name).
Utility:
• Characterizing renal tumor enhancement (relative to the cortex
—• clear cell similar to cortex,
— papillary less than cortex)
- Evaluation of renal arteries and veins
- Optimal phase to detect tumor invasion of the renal veins (important for staging / treatment planning)
Phase can be delayed (last longer) if the kidnevs are shit (failure, renal artery stenosis), obstructed, or in the setting of cardiac failure.
Corticomedullary Phase (CMP)
angio nephrographic - i f you
wanna sound like a pretentious prick
25- 40 Seconds
Contrast in the vascular system and the extracellular interstitial space
Cortex is enhanced the medulla is not (hence the name).
Utility:
• Characterizing renal tumor enhancement (relative to the cortex
—• clear cell similar to cortex,
— papillary less than cortex)
- Evaluation of renal arteries and veins
- Optimal phase to detect tumor invasion of the renal veins (important for staging / treatment planning)
Phase can be delayed (last longer) if the kidnevs are shit (failure, renal artery stenosis), obstructed, or in the setting of cardiac failure.
Nephrographic phase (NP)
70-180 Seconds
Contrast makes its way through the loops of Henle and the collecting tubules (“gets filtered”! Fairly unifonn enhancement of the cortex and medulla
Utility:
• Detect renal tumors
• Especially useful for small / central tumors
Excretory phase (EP)
180 Seconds - 8 Mins
Contrast is excreted into the urinary tract /collecting system
Progressive decrease in the nephrogram (depending on the timing of the exam)
Utility:
• Evaluated morphology of the papilla (necrosis etc…)
• Evaluate for urothelial cell / TCC lesions
Renal Cell Carcinoma
Overview
The most common primary renal malignancy. RCC till proven otherwise: (a) Enhances with contrast (> 15 HU), (b) calcifications in a fatty mass. Risk factors include tobacco use, syndromes like VHL, chronic dialysis (> 3years), family history. These dudes make hypervascular mets. They are ALWAYS lytic when they met to the bones.
Renal Cell Carcinoma
timing
Nephrogram phase
(80 seconds) =
Most sensitive for
detection o f RCC
Renal Cell Carcinoma
pseudoenhancement
A less than 10 HU increase in attenuation is considered within the technical limits of the study and is not considered to represent enhancement. More rare once a cyst is larger than 1.5 cm.
Renal Cell Carcino
can it have fat
Oh yeah, for sure -especially clear cell. This leads to the potential sneaky situation of a fat containing lesion in the liver (which can be a RCC met). Now to make this work they’d have to tell you the patient had RCC - or show you one. A helpful hint is that RCCs with macroscopic fat nearly always have some calcification/ossification - if they don’t it’s probably an AML.
Renal Cell Carcinoma
clear cell
Most common subtype in the general population. This is also the one associated with VHL. It is typically more aggressive than papillary, and will enhance equal to the cortex on corticomedullary phase. The most classic look is a cystic mass with enhancing components.
Renal Cell Carcinoma
papillary
This is the second most common type. It is usually less aggressive than clear cell (more rare subtypes can be very aggressive). They are less vascular and will not enhance equal to the cortex on corticomedullary phase. They also are in the classic T2 dark differential (along with lipid poor AML and hemorrhagic cyst). Risk of primary renal malignancy in the transplanted kidney is six times that of the regular Joe. A point of testable trivia is that these cancers are usually papillary subtypes.
Renal Cell Carcinoma
medullary
Associated with Sickle Cell Trait. It’s highly aggressive, and usually large and already metastasized at the time of diagnosis. Patient’s are usually younger.
Renal Cell Carcinoma
chromophobe
All you need to know is that it’s associated with Birt Hogg Dube.
Conventional RCC Staging:
Stage 1: Limited to Kidney and < 7 cm Stage 2: Limited to Kidney but > 7 cm Stage 3: Still inside Gerota’s Fascia A: Renal Vein Invaded B: IVC below diaphragm C: IVC above diaphragm Stage 4: Beyond Gerota’s Fasica Ipsilateral Adrenal
Syndrome/Association
clear cell
Most common
VHL
Syndrome/Association
papillary
Hereditary appillary renal carcinoma
Transplant kindey
Syndrome/Association
chomophobe
birt hogg dube
Syndrome/Association
medullary
sickle cell trai
Does AD Polycystic Kidney Disease increase your risk for RCC
Well No, but sorta. The genetic syndrome does NOT intrinsically increase your risk. However, dialysis does. Who gets dialysis?? People with ADPKD. It would be such a crap way to ask a question -but could happen. If you are asked, I’m recommending you say no to the increased risk, - unless the question writer specifies that the patient is on dialysis.
Renal Lymphoma
overview
This can literally look like anything. Having said that the most common appearance is bilaterally, enlarged kidneys, with small, low attenuation cortically based solid nodules or masses (“infiltrative soft tissue in the renal hilum ”), and associated lymph nodes. A solitary mass is seen in about 1/4 o f the cases.
Renal Lymphoma
triiva
Out of all the renal masses - lymphoma is the most likely to preserve the normal reniform shape.
Renal Lymphoma
trivia 2
Lymphoma is the most common metastatic tumor to invade / infiltrate the kidneys
Renal Leukemia
The kidney is the most common visceral organ involved. Typically the kidneys are smooth and enlarged. Hypodense lesions are cortically based only, with little if any involvement o f the medulla.
Angiomyolipoma (AML)
thingks to know about them
(1) They are associated with Tuberous Sclerosis — Tuberous Sclerosis can be called Bourneville Disease (for the purpose o f fucking with you)
(2) They can bleed if they get big enough (> 4cm). It’s controversial if they grow or bleed more in pregnancy (if they ask you, I guess you should say yes - because that’s the old knowledge but some modem papers are saying not for sure).
(3) They should never have calcifications (that’s probably a RCC).
(4) They can be lipid poor (about 5% are), and those are T2 dark.
Angiomyolipoma (AML)
gamesmanship
Traditional Spectral Fat Sat or In and Out o f Phase (India Ink) can be used to suggest an AML. Just remember, rarely RCCs can have fat:
renal lesion with fat and calcs
RCC
renal lesion with fat and no calcs
AML
Oncocytoma
overview
This is the second most common benign
tumor (after AML). It looks a lot like a RCC, but has a
central scar 33% of the time (and 100% of the time on
multiple choice). There will be no malignant features (such
as vessel infiltration). They cannot be distinguished from
RCC on imaging and must be treated as RCC till proven
otherwise.
Oncocytoma
imaging
If they want to ask about an Oncocytoma they can show it 3 ways: (1) Solid Mass with central scar - CT or MRI, (2) “Spoke wheel” vascular pattern on US, (3) Hotter than the surrounding renal cortex - on PET CT.
Oncocytoma
gamesmanship
So if you are shown an enhancing renal mass with a central
scar, how do you decide if it’s a RCC or an oncocytoma? The
way to figure it out is simple - just read the mind of the person
who wrote the question. If it’s a practical type then all
enhancing renal masses are RCC till proven otherwise. If it’s
the academic type then central scar = oncocytoma. You may
also think… which of these two people is more likely to
volunteer to write board questions?
Oncocytoma
the pet trick
RCC is typically COLDER
than surrounding renal
parenchyma on PET,
Oncocytoma is typically
HOTTER than surrounding
renal parenchyma on PET,
Oncocytoma trivia
A syndrome associated with bilateral oncocytomas is Birt hogg dube
(they also get chromophobe RCC).
Multilocular Cystic Nephroma
overview
“Non-communicating, fluid-filled locules, surrounded by
thick fibrous capsule.” By definition these things arecharacterized by the absence of a solid component or
necrosis.
Multilocular Cystic Nephroma
buzzword
“protrudes into the renal pelvis.”
The question is likely the bimodal occurrence
(4 year old boys, and 40 year old women).
Multilocular Cystic Nephroma
funny
I like to think of this as the Michael Jackson lesion - it loves young boys and middle aged women.
**Remember this is the “older” nomenclature. It is not the preferred nomenclature dude.
Nerds mined my joke. Now these are “Adult MLCNs” and “Pediatric MLCNs.”
Multilocular Cystic Nephroma
funny
I like to think of this as the Michael Jackson lesion - it loves young boys and middle aged women.
**Remember this is the “older” nomenclature. It is not the preferred nomenclature dude.
Nerds mined my joke. Now these are “Adult MLCNs” and “Pediatric MLCNs.”
Retroperitoneum
ant post anatomy
It is bordered anterior by the anterior pararenal space (black arrows) and posterior by the transversalis fascia (white arrows).
Retroperitoneum
inferior anatomy
Below the level o f the kidneys, there is a blending of the fascial planes which allows for potential spread of
disease between the retroperitoneum and the pelvis. Illustrated with the light grey part (with the black arrows) demonstrating the inferior extension / communication of the retroperitoneum.
retroperitoneum anatomy trivia
The RP contains the lower esophagus, most of the duodenum, the ascending and descending colon, the kidneys, ureters, adrenals, pancreas (minus the tail), aorta, IVC, and the upper 2/3 o f the rectum.
The classic tricks for multiple choice are:
• The pancreatic tail is NOT being part of the RP.
• Lower 1/3 o f the rectum is NOT being part of the RP.
Retroperitoneum Pathology
~75% of the primary retroperitoneal neoplasms are malignant. Any tumor in this location is guilty until proven otherwise. Having said that, there is an enormous amount o f path
that can occur in this location — I’m gonna try and focus on what I think is probably the highest
yield. The chart on the following page does not include adrenal tumors - I’ll cover those in the
endocrine chapter (and peds). RP Fibrosis is mentioned briefly- it is discussed in detail later in
the chapter. Neurogenic tumors will be covered in the neuro chapter.
Retroperitoneum
Lipomatosis
Seen in big fat people - with the classic
history o f “ incomplete bladder emptying”
You can also see this in homeless people, who go to soup kitchens… that
specialize in ice cream soup.
Overgrowth o f benign fat in the pelvis classically perirectal and perivesicular
spaces.
The bladder is displaced anterior and superior - and is “pear shaped” or inverted tear drop shaped.
Retroperitoneum
Liposarcoma
Usually seen in the thigh o f an old person - but is also the most common primary malignant RP in adults.
These things are notorious assholes with a high rate (around 2/3) o f local recurrence — hence the endless surveillance studies you end up reading post treatment.
Don’t call it a comeback (I’ve been here for years - rocking my peers puttin’ suckers in fear). Also - Don’t call it a lipoma - no matter how simple and homogenous it looks.
The deeper a fat containing lesion is - the more likely it is to be a bad actor. Fat-containing retroperitoneal lesions should be thought o f like a male resident on the mammography service- guilty o f all crimes until proven innocent.
Anything that makes them look more complex - calcifications, solid components, not fat sating out - all that makes them even more likely to be bad (not just more likely to be a cancer, but more likely to metastasize).
If you see something you think is a giant fucking AML — but you aren’t totally sure it is coming from the kidney AND it has calcifications - you should think Liposarcoma.
Retroperitoneum
Rhabdomyosarcoma
Most common soft tissue sarcoma in children.
You see a soft tissue mass (in a kid) - you should always be thinking about this.
About h a lf o f them will be in the neck, and about 1/4 o f them in the pelvis around the bladder or testicles.
No surprise - it is gonna look like a
tumor. Heterogenous, enhancing, possibly destroying nearby bone.
Retroperitoneum
Extramedullary hematopoiesisq
Abnormal deposits o f hematopoietic tissue outside the bone marrow.
The look is super nonspecific - just a bunch o f soft tissue masses in the paravertebral region.
History is the only fair way to test this — they have to tell you (or somehow show you) that the patient has a history o f hemoglobinopathy, myelofibrosis, leukemia -
etc…
Retroperitoneum
lymphoma
The Most Common RP malignancy.
Tons o f Big Nodes or a Confluent Soft Tissue Mass. Classically people talk about NHL vs HL.
- NHL nodes are more likely to be larger, noncontinuous, and involve the mesentery.
- HL nodes are more likely to involve the paraaortic region early, and be more continuous
PET/CT is excellent for Lymphoma (in particular it is very useful for disease vs
treated residual scarring — with disease being FDG avid).
Retroperitoneum
Hemorrhage
Most Common Cause = Over-Anticoagulation (high PT/INR)
2nd Most Common Cause = Rupture / Leaking Aorta
3rd Most Common Cause = Bleeding RCC or AML
Retroperitoneum
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
ddx
Lymphoma
Rf fibrosis
erheim chester
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
lymphoma
can displace the aorta forward, and be sen above the renal arteries. tends to push things rather than tether and obstruct
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
rp fibrosis
like lymphom rpf can be hot on pet. it does no usually displace the aorta anterio, is uncommon above the renal arteries and tends to tether and obstruct
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters”
erheim chester
huge zebra. gamesmanship would be to show you plain films of legs with bilateral symmetric sclerosis of the metaphysis (sparing the epiphysis)
Bosniak Cyst Classification:
Class 1: Simple - less than 15 HU with no enhancement
‘Class 2: Hyperdense (< 3 cm). Thin calcifications, Thin septations
‘Class 2F: Hyperdense (> 3 cm). Minimally thickened calcifications (5% chance cancer)
‘Class 3: Thick Septations, Mural Nodule (50% chance cancer)
‘Class 4: Any enhancement (>15 HU)
Hyperdense renal cysts
Basically, if the mass is greater than 70 HU and homogenous, it’s benign (hemorrhagic or proteinaceous cyst) 99.9% of the time.
ADPKD
Kidneys get
progressively larger and lose function (you get dialysis by the 5th decade). Hyperdense
contents & calcified wall are frequently seen due to prior hemorrhage. What you need to
know is: (1) it’s Autosomal Dominant “ADult”, (2) They get cysts in the liver 70% o f the
time, (3) they get seminal vesicle cysts (some sources say 60%), and (4) they get Berry
Aneurysms. As mentioned before, they don’t have an intrinsic risk o f cancer, but do get
cancer once they are on dialysis.
ARPKD
h e s e guys
get HTN and renal failure. The liver involvement is different than the adult form. Instead of
cysts they have abnormal bile ducts and fibrosis. This congenital hepatic fibrosis is
ALWAYS present in ARPKD. The ratio o f liver and kidney disease is inversely related. The
worse the liver is the better the kidneys do. The better the liver is, the worse the kidneys do.
On ultrasound the kidneys are smoothly enlarged and diffusely echogenic, with a loss of
corticomedullary differentiation.
Lithium Nephropathy
Occurs in patients who take lithium long term. Can lead to
diabetes insipidus and renal insufficiency. The kidneys are normal to small in volume
with multiple (innumerable) tiny cysts, usually 2-5 mm in diameters. These “microcysts”
are distinguishable from larger cysts associated with acquired cystic disease o f uremia.
They are probably going to show this on MRI with the history o f bipolar disorder.
Uremic Cystic Kidney Disease
About 40% o f patients with end stage renal
disease develop cysts. This rises with duration o f dialysis and is seen in about 90% in
patients after 5 year of dialysis. The thing to know is: Increased risk of malignancy with
dialysis (3-6x).
Uremic Cystic Kidney Disease
trivia
The cysts will regress after renal transplant.
Von Hippel Lindau
Autosomal dominant multisystem
disorder. 50-75% have renal cysts. 25-50% develop RCC (clear cell).
* Pancreas: Cysts, Serous Microcystic Adenomas, Neuroendocrine (islet cell) tumor
* Adrenal: Pheochromocytoma (often multiple)
* CNS: Hemangioblastoma of the cerebellum, brain stem, and spinal cord
ADPKD vs VHL vs Acquired kidney cysts
ADPKD Cysts in Liver Kidneys are BIG
VHL Cysts in Pancreas
Acquired (Uremic) Kidneys are small
Tuberous Sclerosis
kidneys
Autosomal dominant multi-system
disorder. You have hamartomas everywhere (brain, lung, heart,
skin, kidneys). The renal findings are multiple bilateral
angiomyolipomas. They also have renal cysts, and occasionally
RCC (same rate as general population, but in younger patient
population).
Tuberous Sclerosis
other organs
- Lung - LAM - thin walled cysts and chylothorax
- Cardiac - Rhabdomyosarcoma (typically involve cardiac septum)
- Brain - Giant Cell Astrocytoma, Cortical and subcortical tubers, subependymal nodules
- Renal - AMLs, RCC (in younger patients)
T2 dark renal cyst ddx
Lipid poor aml
hemorrhagic cyst
papillary subtype RCC
Renal MR
Lipid Poor AML
• A small percentage of AMLs are lipid poor in the general population.
• For the purpose of multiple choice - If you see a lipid poor AML (especially if you see a bunch of them)
you need to think about Tuberous Sclerosis - about 30% of their AMLs are lipid poor.
Renal MR
Hemorrhagic cyst
These will likely be T1 bright
Renal MR
Papillary subtype RCC
Dark on T2
- Remember that clear cells (the most common sub-type) are T2 HYPER Intense.
- Both Clear Cell and Papillary will enhance, - but the clear cell enhances more avidly (equal to cortex on cortico-medullary phase).
Multicystic Dysplastic Kidney:
overview
this is the situation where you have multiple tiny cysts forming in utcro from some type of insult.
Multicystic Dysplastic Kidney:
what you should know
- “No functioning renal tissue, ” - shown with MAG 3 exam.
- Contralateral renal tract abnormalities occur like 50% of the time. Typically you think of reflux (VUR) and UPJ Obstructions
THIS vs THAT: MCDK vs Bad Hydro
In hydronephrosis, the cystic spaces are seen to communicate.
In difficult cases renal scintigraphy can be useful. MCDK will show no excretory function.
THIS vs THAT: Peripelvic Cyst vs Parapelvic Cyst
Para (beside): Originates from parenchyma, may compress the collecting
system. These look a lot like the cortical cysts that you see all the time, but
instead of bulging out - they bulge in.
Peri (around): Originates from renal sinus, mimics hydro. If you didn’t
have a pyelogram (delayed) phase - might be tricky to tell apart.
Striated Nephrogram DDx
- Acute ureteral obstruction
- Acute pyelonephritis
- Medullary sponge kidney
- Acute renal vein thrombosis
- Radiation nephritis
- Acutely following renal contusion
- Hypotension (bilateral)
- Infantile polycystic kidney (bilateral)
Pyelonephritis
This is a clinical diagnosis.
However you do end up diagnosing it. It’s
associated with stones. The most common organism
is E. Coli. In acute bacterial nephritis, alternating
bands of hypo and hyperattenuation (striated
nephrogram) are seen. These wedge shaped areas
are related to decreased perfusion. Perinephric
stranding is also commonly seen.
Renal abscess
Pyelo may be complicated by abscess, which can
present on CT as round or geographic low attenuation collections that
do not enhance centrally, but do have an enhancing rim. Bigger than
3cm and these guys might visit the IR section for drainage.
Chronic Pyelonephritis
Sort of a controversial entity. It is not clear whether the
condition is an active chronic infection, arises from multiple recurrent infections, or represents
stable changes from a remote single infection. The imaging findings are characterized by renal
scarring, atrophy and cortical thinning, with hypertrophy o f residual normal tissue. Basically,
you have a small deformed kidney, with a bunch of wedge defects, and some hypertrophied
areas.
Emphysematous Pyelonephritis
This is a life
threatening necrotizing infection characterized by gas formation
within or surrounding the kidney. What you need to know:
(1) it’s really bad, (2) diabetics almost exclusively get it,
(3) echogenic foci with dirty shadowing on ultrasound. If there is air
in the peri-nephric space , that is associated with a miserable shit
outcome.
Next Step:
• Urgent Antibiotics followed by Nephrectomy
Emphysematous Pyelitis
This is less bad relative to emphysematous pyelonephritis.
The gas is localized to the collecting system. It’s more common in women, diabetics, and people
with urinary obstruction. Radiographic finding is gas outlining the ureters and dilated calices.
Pyonephrosis
An infected or obstructed collecting system (which
is frequently enlarged). Can be from a variety o f causes; stones, tumor,
sloughed papilla secondary to pyelonephritis. Can totally jack your
renal function if left untreated. Fluid-Fluid level in the collecting
system can be seen on US. CT has trouble telling the difference
between hydro and pyonephrosis.
Next Step:
• Urgent Decompression (Nephrostomy)
Xanthogranulomatous
Pyelonephritis (XGP)
chronic
destructive granulomatous process that is
basically always seen with a staghom stone
acting as a nidus for recurrent infection. You
can have an associated psoas abscess with
minimal perirenal infection. It’s an Aunt
Minnie, with a very characteristic “Bear Paw”
appearance on CT. The kidney is not
functional, and sometimes nephrectomy is
done to treat it.
Papillary Necrosis
This is ischemic necrosis of the renal papillae, most
commonly involving the medullary pyramids.
Diabetes is the most common cause.
Other important causes include: pyelonephritis
(especially in kids), sickle cell, TB, analgesic use, and
cirrhosis.
Filling defects might be seen in the calyx.
The appearance o f a necrotic cavity in the
papillae with linear streaks o f contrast
inside the calyx has been called a “lobster
d aw sign. ”
Papillary necrosis
trivia
50% of sickle cell patients develop
papillary necrosis
Renal TB
overview
The most common extra-pulmonary site of infection is
the urinary tract. TB in the kidneys is similar to TB in the
lungs with prolonged latency (years after exposure) and
“reactivation.” You could be shown imaging findings that
occur along a spectrum of severity. For the purpose of
multiple choice strategy the more severe disease would lend
itself better to imaging, and the less severe findings would
be more likely to be asked as trivia questions.
Renal TB
imaging
Calyceal blunting (“moth eaten calices”) is the earliest finding. Remember the normal calyx should have a “gentle cup shape” — not all pointy and shit.
Distortion o f the calyx / papillary necrosis will result in
deep cups, and “w” shaped central necrosis patterns.
This is nonspecific - ischemia, diabetes, lots of things can do this
- but it is the “earliest described sign” which makes it testable.
Renal calcifications, which are very common with TB, can be
punctate, curvilinear, or replace the entire kidney. This
extensive calcification is a classic (and very testable) look for
TB - called the “Putty Kidney” - or an autonephrectomized end
stage TB kidney.
Another nonspecific finding - that can help you zero in on the
choice of TB is the presence of multiple calcified mesenteric
lymph nodes — arrows in my cartoon. Calcified adrenal glands
could also be seen.
Renal TB
imaging progression
Normal
calyx distortion/papillary necrosis
progressed necrosis leading to cavity formation. this is the most characteristic sign of renal TB
Focal stenosis of an infundibulum can result in the absence of opacification fo the calyx (phantom calyx)
Infundibulu mstenosis can also be diffuse and result in caliectasis. scarring at the renal pelvis can cause an uplifed appearance and the classic kerr kink at the renal pelvix
ureteral stenosis can cause generalized hydronephrosis
HIV Nephropathy-
overview
This is the most common cause o f renal impairment in AIDS
(CD4 < 200) patients. Although the kidneys can be normal in size, they are classically
enlarged, and bright (echogenic). Some sources will go as far as saying that normal
echotexture excludes the disease (this entity is essentially always is bright). Loss of the renal
sinus fat appearance has also been described (it’s edema in the fat, rather than loss o f the
actual fat).
HIV Nephropathy-
just think
BIG and BRIGHT kidney in HIV positive patient who is clinically in nephrotic
syndrome (massive proteinura).
HIV Nephropathy-
gamesmanship
To show you the kidney is big (longer than 12 cm) they will have
to put calibers on the kidney. Calibers on anything should be a clue that the size
being displayed is relevant.
HIV Nephropathy-
final diagnosis
via biopsy o f the big bright kidney.
Disseminated PCP
renal
n HIV patients can result in punctate (primarily cortical)
calcifications.
CIN
• Allergic reactions are a NOT considered a risk factor for CIN.
• “Risk Factors” for CIN include pre-existing renal insufficiency, diabetes mellitus (even more so with pre-existing renal insufficiency), cardiovascular disease with CHF, dehydration, and myeloma.
• Hydration via IV with 0.9% normal saline 6-12 hours before and continuing 4-12
hours after contrast administration supposedly decreases the incidence o f CIN in patients with chronic renal insufficiency (true mechanism is diluting Cr levels). Oral hydration has been shown to not work as well.
Kidney stones
types
There are several different stone types. The most likely testable trivia for each is:
- Calcium Oxalate - By far the most common type (75%)
- Struvite Stone - More common in women and associated with UTI
- Uric A c id - “Unseen” on x-ray.
- Cystine - Rare and associated with congenital disorders of metabolism
- Indinavir - Stones in HIV patients which are the ONLY stones NOT seen on CT.
Kidney stones
size matters
- Stones measuring 5 mm or smaller have a high likelihood of spontaneously passing.
- Stones measuring 1 cm or larger have a high likelihood of NOT passing spontaneously.
Kidney stones
composition (uric acis vs not uric acid)
Uric acid stones very rarely will require any kind of invasive intervention (lithotripsy,
etc…). The reason is they are very pH dependent. Big Fat People and/or diabetics tend to
have more acidic urine (from all that Mountain Dew) which leads to an increase in uric
acid stones. They can be treated with medical therapy (potassium citrate or sodium
bicarbonate) to increase the pH and melt the stones. You can’t melt a calcium stone by
messing with the pH.
Kidney stones
diagnosis of uric acid stones
Since identification of a uric acid stone is going to change management that makes it a target for trivia on multiple choice. There are 2 things that I would know:
(1) Uric Acid Stones tend to have lower attenuation (< 500 HU).
(2) Uric Acid Stones will have little if any change in H.U. with dual energy CT. The reason is they are composed of “light elements.” The larger atoms (Calcium, Phosphorous, Magnesium, and Sulfur) tend to have a larger change - which is the basis of dual energy CT (80 kv, and 140 kv) identification of stone composition.
Kidney stones
trivia
Trivia: Non Uric Acid Stones will have higher HU at 80 kVp relative to 140 kVp.
Trivia: Uric Acid Stones will be very similar at 80 kVp relative to 140 kVp. *If they do show a small change it will be the opposite - with a slightly higher HU at 140 kVp.
Trivia: Calcium stones are going to show the biggest HU change between high and low energies. In general, low/high energy ratios are going to be around 1.1 for uric acid, 1.25 for cystine, and > 1.25 for calcium.`
Cortical Nephrocalcinosis
This is typically the sequela of cortical necrosis, which can be seen after an acute drop in blood pressure (shock, postpartum, bum patients, etc...).
It starts out as a hypodense nonenhancing
rim that later
develops thin calcifications.
Mimic is disseminated PCP.
Also remember TB can have a
variable calcification pattern as
discussed earlier in the chapter.
Medullary Nephrocalcinosis
Hyperechoic renal papilla / pyramids which may or may not
shadow.
Causes:
• Hyperparathyroidism - Most people will say this is the most common.
• Medullary Sponge Kidney - Some people will say this is the most common.
• Lasix - Common cause in children.
• Renal Tubular Acidosis (distal subtype - type 1)
Trivia: RTA and Hyper PTH - tend to cause a more dense calcification that medullary sponge.
Medullary sponge kidney
A congenital cause of medullary nephrocalcinosis (usually
asymmetric). The underlying mechanism is a cystic
dilation of the collecting tubules of the kidney - so the
testable association with Ehlers-Danlos makes sense. The
association with Carolis also sorta makes sense. The
association with Beckwith-Wiedemann doesn’t really make
sense (and therefore is the most likely to be tested).
Think about medullary sponge kidney with unilateral less
dense medullary’ nephrocalcinosis.
Page Kidney
This is a subcapsular hematoma which
causes renal compression and complex fuckery with the renin-angiotensin system. The result is hypertension.
The capsule is the real issue here. That
capsule is tough and won’t expand so the hematoma puts the squeeze on the “meat” of the kidney. You could never get a “pagepancreas” because the pancreas has no capsule. This is the same reason why resistive indices are worthless in a pancreas Subcapsular Hematoma + HTN = Page(no capsule) but sometimes useful in a kidney (which has a capsule).
Subcapsular Hematoma + HTN
Page
Page kidney classic clinical history
htn post biopsy lithotripsy or trauma
Delayed Nephrogram
One kidney enhances and the other doesn’t (or does to a lesser
degree). Basically this is happening from pressure on the kidney, either extrinsic from a
Page kidney situation, or intrinsic from an obstructing stone.
Persistent Nephrogram
This is seen with hypotension/shock and ATN. They can show
this two ways, the first would be on a plain film of the abdomen (with dense kidneys), the
second would be on CT. The tip offs are going to be that they tell you the time (3 hours
etc…) and it’s gonna be bilateral.
Renal Infarct
overview
So wedge shaped hypodensities in the kidney can be seen with lots o f stuff (infarct, tumor,
infection, etc…)- Renal infarcts are most easily identified on post contrast imaging in the
cortical phase. If the entire renal artery is out, well then it won’t enhance (duh).
Renal Infarct
cortical rim sign
which is absent
immediately after the insult, but is seen 8 hours
to days later. You have a dual blood supply,
which allows the cortex to stay perfused.
Renal Infarct
flip flop enhancement
can be seen
where a region o f hypodensity / poor
enhancement on early phases becomes
relatively hyperdense on delayed imaging.
Renal Vein Thrombosis
Numerous causes; including dehydration, indwelling umbilical venous catheters (most
common in neonates), and nephrotic syndrome (most common in adults). This can mimic a
renal stone; presenting with flank pain, an enlarged kidney, and a delayed nephrogram.
On Doppler they are going to show you Reversed arterial diastolic flow and absent venous
flow.
T r a n s p l a n t
kidney overview
Renal transplant is the best treatment for end stage renal disease, and the quality of life is
significantly better than that of a long term dialysis patient (which fucking sucks !!!). The
transplanted kidney is most commonly placed in the extraperitoneal iliac fossa so that the
allograft can be anastomosed with the iliac vasculature and urinary bladder.
The way they do this surgery depends on where the kidney comes from (living vs cadaveric). The
main thing to know is that a kidney “harvested” from a hobo found floating in the river will have
not only the kidney and renal artery removed but also a segment of the aorta - that can be used for
end-to-side anastomosis to the recipient external iliac artery. In a living donation they aren’t gonna
carve on the aorta (cuz you need your aorta to live). In both cases, end to side anastomosis is
preferred for the vein and artery - typically to the external iliac vein and artery (although you can
see the internal iliac used in some situations).
transplant normal kidney flow
The superficial location of the transplant in the iliac fossa makes ultrasound the
modality of choice for evaluation. A transplant kidney is just like a native kidney. It should
have low resistance (it’s always “on”). The upstroke should be brisk, and the flow in diastole
forward (remember it’s always “on”).
Understanding renal RIs
There are two major points to know first when thinking about RIs. The first is the kidney has
a capsule, and that capsule is unforgiving (it believes in nothing Lebowski). The second is a
sick kidney is a swollen kidney.
Peak Systolic - End Diastolic “lowest diastolic”
Now lets look at this formula: ™ =
Peak Systolic
If the meat (parenchyma) of the kidney
is sick and swollen, but can’t expand
because it is wrapped in a tight
unforgiving capsule you can imagine
the blood vessels going through that
kidney are going to get the squeeze.
You can also probably imagine that the
passive diastolic flow would be more
impaired (compared to the active
systolic flow) by this squeeze.
If the meat of the kidney becomes
“sick” from whatever the cause might
be (rejection, infection, inflammation,
etc…) it swells increasing resistance.
RI’s should stay below 0.7. The higher the RI the sicker the kidney. This is why RIs are useful,
and this is why an upward trend in RI is worrisome. It is important to remember, RIs are not
specific since elevation occurs with basically every pathology. For the purpose of multiple
choice, you should never use elevated RIs to exclude answers (unless the answer is normal).
Elevation in RIs does tell you something is wrong, especially if there is an upward trend.
Urologic complication in transplant kidney
Obstruction
The ureter must also be surgically implanted (ureteral neocystostomy to the bladder
dome). Just like in a native kidney the ureter can get obstructed. Don’t be fooled by the ultimate asshole trick o f
showing you mild hydro on a transplant (especially one with normal labs) and trying to get you to call obstruction.
Transplanted kidneys pretty much all have some mild hydro - this is related to denervation o f the transplant, and
floppy tone to the ureter. If there is a true obstruction it is usually at the site o f ureteral implantation to the bladder.
The common causes are post operative edema, scarring, or technical errors leading to kinking. Stones, clots, etc.. are
less common. Having said that - transplants are more likely to have stones compared to the general population - it is
just that other stuff (edema, scar, kink , e tc … is more common).
Urologic complication in transplant kidney
hematoma
Common immediately post op. Usually resolves spontaneously. Large hematoma can produce
hydro. Acute hematoma will be echogenic, and this will progressively become less echogenic (with older
hematomas more anechoic and septated).
Urologic complication in transplant kidney
urinoma
This is usually found in the first 2 weeks post op. Urine leak or urinoma will appear as an
anechoic fluid collection with no septations, that is rapidly increasing in size. Most leaks (urine extravasation)
are going to be at the ureterovesical anastomosis. MAG 3 nuclear medicine scan can be used to demonstrate
this (or the cheaper ultrasound).
Urologic complication in transplant kidney
lymphocele
Lymphoceles typically occur 1-2 months after transplant. They are caused by leakage of
lymph from surgical disruption o f lymphatics or leaking lymphatics in the setting o f inflammation. The fluid
collection is usually medial to the transplant (between the graft and the bladder). They are actually the most
common fluid collection to cause transplant hydronephrosis.
ipsilateral lower edema from femoral vein compression
Hematoma post op renal transplant
overview
Immediate Post Op — Till about 1 week
Think Complex Collection
Heterogenous, Septa, Etc…
CT: Appearance will depend on how acute it is. Acute = more dense.
MRI: T1 Bright (usually)
urinoma post op renal transplant
overview
Around Day 10
Think Simple Collection between the bladder and the kidney
CT: If you do a delayed phase you can see leakage o f contrast
Nukes: Tracers like MAG3 and DTPAwill accumulate outside the expected location o f the bladder.
Fluid Cr > Serum Cr
Fluid K+ > Serum K+
These things happen from ischemia to the ureter or obstruction (usually)
abscess post op renal transplant
overview
Weeks to Months
Think Complex Hyperemic Collection
CT: Peripheral Enhancement
US: Hyperemia (increased flow at the periphery)
Fever and Elevated WBC would be obvious clues - although I expect the assholes would deliberately withhold that information
lymphocele post op renal transplant overview
2 weeks - 6 Months
Think Simple Collection (may have tiny septa).
CT: If you do a delayed phase you will NOT see leakage of contrast
Nukes: Tracers like MAG3 and DTPA will NOT accumulate outside the expected location o f the bladder.
Fluid Cr ~ Serum Cr
Fluid K+ ~ Serum K.+
They will Not usually drain these things (they ju st come back). If they do opt to treat them its usually via sclerosing agent.
Renal transplant
rejection overview
Rejection is complicated business with a bunch of fancy sounding French words (maybe Latin)
associated with numerous overlapping biopsy related classification criteria and which subtype of
the T-Cell mediated pathway blah blah blah. None of that shit matters to Radiologists. Rejection
workup involves, labs, considering the time interval, ultrasound, maybe nukes, and in many
cases a biopsy to actually prove it.
Renal transplant
hyperacute rejection
is an immediate failure of the graft - and you rarely see this
imaged. It is basically a dead on arrival transplant.
Renal transplant
acute rejection
usually seen around week 1-3 (it is actually rare in the first 3 days).
There is overlap between the antibody mediated types (which occur early) and the T-cell
activated types (which occur later) - but again that shit is irrelevant to Radiologists. Up to 20% of
transplant patients will have some early rejection. The graft may swell and Rls will go up.
Rejection vs ATN is the common question - and MAG3 can help (see chart on the next page).
Regardless o f the Nukes Exam, most sources say “biopsy” is the standard for differentiating the
two.
Renal transplant
acute tubular necrosis
common and occurs to variable degrees on basically
every transplant. The mechanism is ischemia in the kidney after they carve it out o f the Hobo
(presuming the transplant is from the usual donor - Hobo found floating in the river). So in the
time it takes to carve it out of the Hobo and sew it into an affluent celebrity (Selena Gomez,
Tracy Morgan, etc..) there is going to be some ischemia - and therefore ATN.
Lingo: “Delayed Graft Function (DGF) ” = transplant requiring dialysis in the first week. The
amount of “cold ischemia” (how long the hobo kidney is on ice) is said to be the best predictor.
Renal transplant
cyclosporin toxicity (calcineurin inhibitor)
Immunosuppressive therapy
necessary to keep the body from rejecting the graft can ironically end up poisoning the graft.
The timing is usually later than ATN (around a month). The MAG3 exam can also look like
ATN (normal perfusion, with retained tracer) but will NOT be seen in the immediate post op
period.
Renal transplant
chronic rejection
gradual progress process which occurs months to years after
transplant. The kidney may enlarge, and you can lose corticomedullary differentiation. The Rls
will elevate (> 0.7), which is nonspecific.
Acute rejection
US RI
mechanism
timing
mag3-flow
mag3 uptake
mag3 making piss
US RI elevated
mechanism antibody cell mediated
timing first week
mag3-flow crap
mag3 uptake crap/delayd
mag3 making piss crap slow progressive excretion
ATN
US RI
mechanism
timing
mag3-flow
mag3 uptake
mag3 making piss
US RI elevated
mechanism ischemia during harvesting
timing first week
mag3-flow normal to mild delay
mag3 uptake pretty much normal
mag3 making piss crap slow progressive excretion
Cyclosporin toxicity
US RI
mechanism
timing
mag3-flow
mag3 uptake
mag3 making piss
US RI elevated
mechanism nephrotoxin reaction to immunosuppressive
timing month
mag3-flow normal to mild delay
mag3 uptake pretty much normal
mag3 making piss crap slow progressive excretion
Chronic rejection
US RI elevated
mechanism cellular immune t cell mediated
timing months
mag3-flow crap
mag3 uptake crap/delayed
mag3 making piss crap slow progressive excretion
Renal transplant renal artery thrombosis
Almost always seen within the first month (usually minutes to
hours post opt, resulting from technical factors - kinking or torsion of the vessel. Unless the patient
is undergoing rejection, or has renal artery stenosis (which has progressed to full on thrombosis) it is
pretty fucking rare to see this outside the early post-operative period. As a point of trivia - this is
different than hepatic artery transplant thrombosis — which is described as a later complication ( >
than 1 month post op) — so don’t get it twisted and let the bastards trick you.
Renal transplant
Renal Artery Stenosis
Typically seen within the first year after transplant (usually weeks
to months). Easily the most common vascular complication o f transplant. This usually occurs at
the anastomosis (especially end-to-end types). CMV is a risk factor. The clinical / scenario buzzword
is going to be “refractory hypertension.”
Renal transplant
renal artery stenosis criteria
- PSV > 200-300 cm/s. (some people say 340-400 cm/s)
- PSV ratio > 1.8-2.5x (Stenotic Part vs Non Stenotic Part)
- Tardus Parvus: Measured at the Main Renal Artery Hilum (NOT at the arcuatcs)
- Anastomotic Jetting
Renal transplant
renal vein thrombosis
Typically seen within the first week. Typically the kidney is
swollen. Instead of showing you the Doppler of the renal vein (which would show no flow), they will
most likely show you the artery, which classically has reversed diastolic flow.
Renal transplant
avf
These occur secondary to biopsy. They occur about 20% of
the time post biopsy, but are usually small and asymptomatic. They will likely show it with tissue
vibration artifact (perivascular, mosaic color assignment due to tissue vibration), with high arterial
velocity, and pulsatile flow in the vein.
Renal transplant
pseudoaneurysm
These also occur secondary to biopsy, but are less common. They can also
occur in the setting of graft infection, or anastomotic dehiscence. They will most likely show you the
classic “yin-yang” color picture. Alternatively, they could show Doppler with biphasic flow at the
neck of the pseudoaneurysm.
Renal transplant
renal allograft compartment syndrome
overview
Seen immediately - usually < 2 hours post transplantation
This is usually an operative complication where the kidney was too big for the pelvic extraperitoneal space they decided to jam it and when they stitch the fascia back up it puts the squeeze
on the kidney. You can imagine if there was a fluid collection nearby that would
make it worse
Doppler: Absent or almost totally absent cortical flow in the kidney (color or
power Doppler)
Transplant Size matters - a large transplanted kidney is the main risk factor associated with RACS.
Renal transplant
Renal vein thrombosis overview
Usually the first 5 days (peak at 48 hours)
Depending on who you ask - like 30% o f kids have graft failure because o f this…
The incidence is less that RAS - but the morbidity associated with it is still high.
Doppler: Flow in the vein is gone. Reversed diastolic arterial flow.
Grey Scale: Swollen /enlarged kidney.
Renal transplant
Renal artery stenosis overview
3 months to 2 years depending on who you ask
Depending on who you ask - this is the most common vascular complication in a transplant.
Classic History is “hypertension refractory to treatment”
The lesion is usually at the level o f the surgical anastomosis.
Doppler: PSV > 250 cm/s or 1.8-2.5x increase from the “normal” vessel.
There is a trend towards using 340-400 cm/s for a more specific call. Which number will the test writer want you to use? Simply read his or her mind to find out and answer accordingly.
Rx: Most places will try and angioplasty the stenosis first. Having said that, if it is right over the anastomosis - you will hear people say surgery might be safer / better (higher risk of ripping the thing in half when you stretch it)
Renal transplant
renal artery thrombosis overview
Usually very early (mins to hours) as a post op complication (clamp injury etc…)
It is rare to see this late (in the absence o f progressive stenosis or raging rejection)
Doppler: Flow is gone
Grey Scale: Might see wedge shaped hypoechoic infarcts
Renal transplant
occuring at anytime after trauma or procedure
av fistula
pseudoaneurysm
traumatic hematoma
Renal transplant
av fistula overview
Feeding artery with a high velocity low resistance waveform
Vein with a turbulent arterial appearance.
Tissue Vibration Artifact
Usually - no clinically significant hemodynamic consequence and no intervention needed
Renal transplant
pseudoaneurysm overview
To-and-Fro pattern of blood flow within the neck
Yin-yang sign o f swirling blood within the sac
Often need an intervention - especially i f large (historically > 2 cm) or increasing in size
Renal transplant
Traumatic hematoma
This can occur after biopsy or from blunt trauma.
Transplant kidneys don’t have ribs and are fairly superficial - so they can get banged up in minor trauma.
Complex Collection
Heterogenous, Septa, Etc…
Transplant kidney Renal cancer
risk of new cancer
The prolonged immunosuppression therapy that renal transplant patients are on places them
at significantly (lOOx) increased risk o f developing some type o f cancer. In particular, they
get more nonmelanomatous skin cancer, lymphoma, and colon cancer. In fact - annual skin
exams are a recommendation for all renal transplant patients — that is kinda random …. and
possibly testable.
Transplant kidney
RCC
Increased risk, with most o f the cancers (90%) actually occurring in the native
kidney. Etiology is not totally understood; maybe it’s the immunosuppression or the fact that
many transplant patients were on dialysis (a known risk factor) that leads to the cancer risk.
In reality it doesn’t matter, and is probably both.
Risk o f primary renal malignancy in the transplanted kidney is six times that o f the regular
Joe. A point o f testable trivia is that these cancers are usually papillary subtypes.
Transplant kidney
Post Transplant Lymphoproliferative Disorder (PTLD)
This is an
uncommon complication of organ transplant, associated with B-Cell proliferation. EBV is a
risk factor and that is one o f the main reasons they screen for it - and will put people on
Rituximab (if they mention that drug - they could be hinting that patient was EBV positive).
It is most common in the first year post transplant, and often involves multiple organs. The
most typical look is a mass lesion encasing / replacing the hilum - although the appearance is
notoriously variable. The treatment is to back off the immunosuppression.
Renal Transplant + BK Virus = Urothelial Malignancy
WTF is “BK Vints ” ? It is some random virus that pretty much everyone gets and doesn’t even
notice. Nephrologists love to write papers on this critter. Supposedly… (yes I read their stupid
papers) it is usually the donor kidney that has it and then it reactivates something crazy once the
patient is immunosuppressed. Sometimes it even mimics rejection.
Just know BK = Urothelial Cancer.
Transplant kidney
cyclophosphamide
As a point of trivia, significant exposure to cyclophosphamide
(less common now with the development of cyclosporin A) is associated with increased risk
of urothelial cancer.
Renal trauma gamesmanship
A good “Next Step” type question in the setting o f renal trauma
(or pelvic fracture) would be to prompt you to get delayed imaging - this is helpful
to demonstrate a urine leak.
Fractured kidney
A laceration, which extends
the full depth of the renal parenchyma. By definition the
laceration must connect two cortical surfaces - so think
about it going all the way through.
Shattered kidney
This is a more severe form of
a fractured kidney. A kidney with 3 or more fragments -
this is the most severe form o f renal fracture.
Renal Wedge Shaped Perfusion
Abnormality
thinsk segmental artery injury
renal diffuse nonperfusion
think devascularized kidney
Renal persistant nephrogram
thingk renal vein injury/thrombosis
renal trauma trivia
A transplant kidney is at increased risk o f injury in most trauma because of its superficial
location (and loss o f the normal rib protection).
ureteral stones
Stones tend to lodge in 3 spots: UPJ, UVJ, pelvic brim.
Ureteral Wall Calcifications
Wall calcifications should make you think about two things: (1) TB, (2) Schistosomiasis (worms).
Ureteritis cystica
Numerous tiny subepithelial fluid-filled cysts within the wall of
the ureter. The condition is the result o f chronic inflammation (from stones and/or chronic
infection). Typically this is seen in diabetics with recurrent UTI. There may be an increased
risk of cancer.
Ureteral pseudodiverticulosis
This is similar to ureteritis cystica in that both
conditions are the result o f chronic inflammation (stones, infection). Instead of being cystic
filling defects, these guys are multiple small outpouchings. They are bilateral 75% of the
time, and favor the upper and middle third. There is an association with malignancy.
malokoplakia
overview
( “The Accursed”) - Former Lord o f the Dark Elves of Svartalfheim and rare chronic granulomatous condition, this pathology can create soft tissue nodularity /plaques in the bladder and ureters (bladder more often). It is seen in the setting of chronic UTIs (highly associated with E.Coli). often in female immunocompromised patients. There is also a more remote association with the Casket o f Ancient Winters. Since malakoplakia most frequently manifests as a mucosal mass involving the ureter or bladder, the most common renal finding is obstruction secondary to a lesion in the lower tract. Step
1 buzzword = Michaelis-Gutmann Bodies.
Leukoplakia =
premalignant
malakoplakia =
not premalignant
malakoplakia most easily tested piece of trivia
Not premalignant and usually gets better with antibiotics
Leukoplakia overview
This is essentially squamous metaplasia secondary to chronic irritation
(stones or infections). The bladder is more commonly involved than the ureter. Imaging
findings are unlikely to be shown, but would be mural filling defects.
Leukoplakia most easily tested trivia
is considered premalignant and the
cancer is squamous cell.
Leukoplakia
trivia
associated with squamous cell carcinoma NOT transitional cell
Retroperitoneal Fibrosis
overview
This condition is characterized by proliferation o f aberrant fibro-inflammatory tissue, which
typically surrounds the aorta, IVC, iliac vessels, and frequently traps and obstructs the
ureters. It is idiopathic 75% o f the time. Other causes include prior radiation, medications
(methyldopa, ergotamine, methysergide), inflammatory causes (pancreatitis, pyelonephritis,
inflammatory aneurysm), and malignancy (desmoplastic reaction, lymphoma).
Retroperitoneal Fibrosis
trivia
- Mostly (75 %) idiopathic AKA“Ormond Disease”
• Associated with IgG4 disorders (autoimmune pancreatitis, Riedel’s thyroiditis, inflammatory pseudotumor)
• Classically shown with medial deviation o f ureters
• It’s more common in men - Malignancy associated RP fibrosis occurs about 10% o f the time (some people advocate
using PET to find a primary) - The Fibrosis will be Gallium avid, and PET hot in its early stages and cold in its late stages (mirroring its inflammatory stages). Metabolically active RP fibrosis will show increased FDG and Gallium uptake, regardless o f a benign or malignant underlying cause
Subepithelial Renal Pelvis Hematoma:
overview
This tends to occur in patients on long-term anticoagulation or a history o f hemophilia. You are going to have a thickened upper tract wall - which is a classic mimic for TCC.
Subepithelial Renal Pelvis Hematoma:
gamesmanship
would expect pre and post contrast images so that you can make the classic findings o f hyperdense clot on the pre-contrast that does NOT enhance. Although a non-contrast alone (showing blood in the urinary pelvis) with the history of hemophilia should also be enough to seal the deal.
LAteral deviation of the ureters
Retroperitoneal Adenopathy
Aortic Aneurysm
Psoas Hypertrophy (proximal ureter)
medial deviation of the ureters
Retroperitoneal Fibrosis
Retrocaval Ureter (right side)
Pelvic Lipomatosis Psoas Hypertrophy (distal ureter)
Transitional Cell Carcinoma (Urothelial Carcinoma)
high yield trivia
a way to remember this is where ever the urine sits static the longest is more likely to have the cancer.
So: Bladder > Renal Pelvis > Ureter. If you are getting cancers in the
ureter than you probably also have them in the bladder
• Ureter is the least common location for TCC of the urinary tract
• TCC of the renal pelvis is 2x -3x times more common than ureter
• TCC of the bladder is lOOx times more common than ureter
• In the ureter 75% of the TCCs are in the bottom 1/3
• If you have upper tract TCC there is a 40% chance of developing a bladder TCC
• If you have bladder TCC there is a 4% chance of developing a Renal Pelvis or Ureteral TCC
• Ureteral TCC is bilateral 5%
Transitional Cell Carcinoma (Urothelial Carcinoma)
risk factors
- Smoking
- Azo Dye
- Cyclophosphamide
- Aristolochic acid (Balkan Nephropathy - see below)
- Horseshoe Kidney
- Stones
- Ureteral Pseudodiverticulosis
- Hereditary Non-Polyposis Colon Cancer (type 2)
Balkan Nephropathy
This is some zebra degenerative nephropathy endemic to
the Balkan States. The only reason I mention it is that it has a super high rate of renal pelvis and upper ureter TCCs. It’s thought to be secondary to eating aristolochic acid (AA) in seeds of the Aristolochia clematitis plant (herb).
Squamous Cell
ureter
This is much less common than TCC (in the US anyway). The major predisposing factor is schistosomiasis (they both start with an “S”).
Hematogenous Metastasis
ureter
Mets to the ureters are rare but can occur (GI, Prostate, Renal, Breast). They typically infiltrate the periureteral soft tissues and demonstrate transmural
involvement.
Fibroepithelial Polyp
ureter
This is a benign entity presents as a filling defect in the renal pelvis or proximal ureter - which mimics a TCC (blood clot or radiolucent stone). The diagnosis is typically made post nephrectomy - since the assumption is nearly always TCC.
Fibroepithelial polyp
gamesmanship
For the purpose of multiple choice (and real life), renal pelvis filling defects should always be assumed to be either clot, calcium (stone), or cancer. The only way I can think that a polyp question could be ask would be something like “which features would make a polyp more likely?” It has to be a trivia question, they couldn’t (in good conscious) expect you to pick polyp over TCC with imaging alone — even if the findings and demographics were perfect - that would be teaching a terrible clinical message.
This vs that polyp vs tcc
polyp
younger 30-40
smooth/oblong
mobile
This vs that polyp vs tcc
tcc
older 60-70
irregular
fixed
Bladder development anomalies
prune belly (eagle barrett syndrome)
This is a malformation triad which occurs in males. Classically
shown on a babygram with a kid shaped like a pear (big wide
belly).
Bladder development anomalies
prune belly triad
• Deficiency of abdominal musculature
• Hydroureteronephrosis
• Cryptorchidism
(bladder distention interferes with descent o f testes)
Bladder development anomalies
urachus
This is also discussed in the Peds chapter. I will briefly mention that the primary concern is the development of a midline adenocarcinoma. Most of the time the presence of a midline mass makes
it obvious although calcification within any urachal soft tissue should
make you think cancer.
bladder diverticula
These are more common in boys, and can be seen in a few situations. Most bladder diverticula can also be acquired secondary to chronic outlet obstruction (big prostate). There are a few syndromes (Ehlers Danlos is the big testable one) that you see them in as well.
bladder ears
“Transitory extraperitoneal herniation of the bladder” if you want to sound
smart. This is not a diverticulum. Instead, it’s transient lateral protrusion of the bladder into the
inguinal canal. It’s very common to see, and likely doesn’t mean crap. However, some sources
say an inguinal hernia may be present 20% of the time. Smooth walls, and usually wide necks can
help distinguish them from diverticula.
bladder ears
“Transitory extraperitoneal herniation of the bladder” if you want to sound
smart. This is not a diverticulum. Instead, it’s transient lateral protrusion of the bladder into the
inguinal canal. It’s very common to see, and likely doesn’t mean crap. However, some sources
say an inguinal hernia may be present 20% of the time. Smooth walls, and usually wide necks can
help distinguish them from diverticula.
Bladder Cancer
gamesmanship
GROSS hematuria confers a 4x greater risk than microscopic hematuria. If the question header specifically indicates “GROSS” hematuria - think bladder cancer first.
Bladder Cancer
next step
Along these lines if the history is GROSS hematuria, and the patient is 50 or older
they should get a CT Hematuria Protocol / Urography (pre and post, with delays), and also cystoscopy.
Bladder Cancer
what does marcelus walls bladder cancer look like
Short answer = soft tissue in the bladder. If you are looking at a well distended bladder (which is pretty much required to say shit about the bladder) focal wall thickening or nodules should be considered cancer till proven otherwise.
Bladder Cancer
what about diffuse circumferential bladder wall thickening
This isn’t usually cancer, especially in
the world of multiple choice. This is probably more of an inflammation or infection situation - or chronic
partial outlet obstruction (if the prostate is enormous). I’d only call a cancer in this situation if there was
really asymmetric nodular thickening superimposed on circumferential thickening.
Bladder Cancer
what about enhancement
You will hear people refer to bladder cancers as hypovascular tumors - but
they can and often do enhance, especially on early arterial phases. Any focal enhancement should trigger
you to think cancer - unless you’ve got good reasons to think otherwise. Having said all that - most
people will say the delayed phase is the most important for identifying bladder cancers - and that is the
choice I would recommend if you are forced to choose (white background of contrast - makes soft tissue
masses easier to see).
Bladder Cancer
types of cancer/mimics
rhabdomyosarcoma
This is the most common bladder cancer in humans less than 10 years of age. They arc often infiltrative, and it’s hard to tell where they originate. “Paratesticular Mass” is often a
buzzword. They can met to the lungs, bones, and nodes. The Botryoid variant produces a polypoid
mass, which looks like a bunch of grapes.
Bladder Cancer
types of cancer/mimics
tcc
As stated above, the bladder is the most
common site, and this is by far the most common subtype. All the risk factors, arc the same as above.
If anyone asks “superficial papillary” is the most common TCC bladder subtype.
Bladder Cancer
types of cancer/mimics
scc
When I say Squamous Cell Bladder, you say Schistosomiasis. This is
convenient because they both start with an “S.” The classic picture is a heavily calcified bladder and
distal ureters (usually shown on plain film, but could also be on CT). Another common association
with squamous cell cancer of the bladder in the presence of a longstanding Suprapubic catheter. This
also starts with an “S.”
Bladder Cancer
types of cancer/mimics
adenocacinoma
This is a common trick question. When I say Adenocarcinoma of
the Bladder, you say Urachus. 90% of urachal cancers are located midline at the bladder dome.
Bladder Exstrophy is also associated with an increased risk of adenocarcinoma.
Bladder Cancer
types of cancer/mimics
leiomyoma (bladder fibroid)
Benign tumor (not cancer - even though this section is bladder cancer) its often indicentally discovered (most common at the trigone)
most common benign bladder tumor
looks like a fibroid (smooth, solid, homogenous)
clinical buzzword urinary hesitance or dribbling
TCC bladder cancer overview
high yield
By far the Most Common Type (like 90%)
Smoking is the classic risk factor, but other poisons including arsenic, aniline, benzidine - etc or as they call it in Flint Michigan “Tap Water” - have a documented relationship
Bladder Diverticulum - 2-10% increased risk (related to stasis). In this setting early perivesical fat invasion is classic (because a diverticulum has limited muscle in the wall to slow the invasion)
Favors the base (inferior posterior)
Sub-divided into Papillary vs Non Papillary.
Papillary ones look like shrubs “frond like ” and tend to be low grade.
Non-Papillary tends to be more aggressive.
SCC bladder cancer
high yield
Second Most Common Type (like ~ 8%)
Classic Associations:
• Recurrent urinary tract infections and stone disease
• Schistosoma Hematobium (asshole jungle worm)
• Longstanding Suprapubic Catheter
This is convenient because they both start with an “S.”
The classic picture is a heavily calcified bladder and distal ureters (usually shown on plain film, but could also be on CT).
Tumor favors the trigone and lateral walls
The ones NOT associated with Schistosomiasis tend to be more aggressive.
adenocarcinoma bladder cancer
high yield
Third Most Common Type (like 2%)
Classic Associations:
• Urachal Remnant
• Bladder Exstrophy 90% of urachal cancers arc located midline at the bladder dome.
The classic picture is a large midline mass associated with a urachal remnant with scattered calcifications.
70% of cases have calcification (if you see calcifications in a urachal remnant it should make you think about an early cancer).
Rhabdomyosarcoma bladder cancer
high yield
Most common bladder tumor in Peds.
They are often infiltrative, and it’s hard to tell where they originate.
Paratesticular Mass” is often a buzzword.
They can met to the lungs, bones, and nodes.
The classic look is Grape-like polypoid masses — this is the sarcoma botryoides variant
Diversion Surgery
overview
After radical cystectomy for bladder cancer there are several urinary diversion procedures that
can be done. People generally group these into incontinent and continent procedures. There
are a ton o f these (over 50 have been described). I just want to touch on the big points, and
focus on complications (the most testable subject matter). The general idea is that a piece of
bowel is made into either a conduit or reservoir, and then the ureters are attached to it.
