4. Genitourinary (Kidneys) Flashcards

1
Q

Normal kidney anatomy (4)

A

Normal adult kidney is bean shaped, with smooth, oftem lobulated outer border.
Surrounded by thick capsule, outlined by perirenal fat.
Perirenal fat is continguous with the renal sinus, filling the middle of the kidney.
Cortex extends centrally into the middle of kidney, separated by less echogenic medullary pyramids.
Normal kidney is around 9-15cm in length.

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2
Q

Normal kidney - ultrasound (3)

A

Echogenicity should be equal to, or slightly less, than liver and spleen.
If renal echogenicity > liver, suggests impaired renal function.
Liver > kidney suggests fatty liver.

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3
Q

Fetal lobulation (3)

A

Anatomic variant.
Fetal kidneys are subdivided into lobes, separated with grooves.
Sometimes this lobulation persists into adulthood.

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4
Q

Fetal lobulation vs Scarring (2)

A

Lobulation: Renal surface indentations overlie the space between pyramids.
Scarring: renal surface indentations overlie medullary pyramids.

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5
Q

Dromedary hump (2)

A

Anatomic variant.
Focal bulge on left kidney, forms as a result of adaptation to adjacent spleen.

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6
Q

Prominent or hypertrophied column of Bertin (3)

A

Normal variant, hypertrophied cortical tissue located between pyramids results in splaying of the sinus.
Other than hypertrophy, looks and enhances normally.
Looks like big echogenic cortex on US.

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7
Q

Renal agenesis (4)

A

Congenital absence of one or both kidneys.
Unilateral can be asymptomatic.
- usually sporadic, but can be associaed with gynae abnormalities such as unicornate uterus
- in men, can be associated with absence of ipsilateral epididymis and vas deferens, or ipsilateral seminal vesicle cyst
Bilateral can cause Potter sequence.

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8
Q

Renal agenesis - associations (5)

A

Potter sequence
- Insult (maybe ACEi) > Kidneys don’t form > Can’t pass urine > Can’t develop lungs (Pulmonary hypoplasia)
Mayer-Rokitansky-Kuster-Hauser
- Mullerian duct anomalies including absence or atresia of uterus.
- Associated with unilateral renal agenesis
Lying down adrenal or “pancake adrenal” sign
- Elongated appearance of adrenal, not normally molded by adjacent kidney.
- Can differentiate surgically absent vs congenitally absent kidney.

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9
Q

Horseshoe kidney (8)

A

Most common fusion anomaly.
Complications include
- traumatic injury (gets crushed against vertebral body)
- UPJ obstruction
- Recurrent infection
- Recurrent stones
- Wilms tumour (8x increased risk)
- TCC due to infections
Also associated with
- Turners
- Renal carcinoid

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10
Q

Crossed fused renal ectopia (3)

A

One kidney comes across the midline and fuses with the other.
Ectopic Crossed Kidney is Inferior.
Left kidney more commonly crosses.
Complications include stones, infection and hydronephrosis.

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11
Q

Renal cell carcinoma - overview (8)

A

Commonest primary renal malignancy.
RCC until proven otherwise if:
- Enhances >15HU with contrast
- Calcifications in a fatty mass
Risk factors include
- Tobacco
- VHL
- Chronic dialysis (>3 years)
- Family Hx
Hypervascular mets, mets are always lytic when they met to bone.

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12
Q

Pseudoenhancement (2)

A

Less than 10HU is considered within technical limits of study and not necessarily enhancement.
More rare once a cyst is larger than 1.5cm

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13
Q

Fat in RCCs (3)

A

Clear cell most likely to have fat.
Fat containing lesion in the liver can be RCC met.
RCCs with macroscopic fat almost always have some calcification, otherwise it’s likely an AML.

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14
Q

RCC subtypes (8)

A

Clear cell
- most common, associated with VHL.
- More aggressive than papillary and will enhance equal to cortex on corticomedullary phase
Papillary
- second commonest. Less agressive than clear cell.
- Less vascular and will not enhance equal to corrtex on corticomedullary phase.
- T2 dark, along with lipid poor AML and haemorrhagic cysts.
Medullary
- Associated with sickle cell trait.
- Highly aggressive and usually large, usually already mets at time of diagnosis. Usually younger patients.
Chromophobe
- Associated with Birt Hogg Dube

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15
Q

RCC staging (7)

A

Stage 1 = Limited to kidney, >7cm
Stage 2 = Limited to kidney, >7cm
Stage 3 = Still inside Gerota’s fascia
Stage 3a = Renal vein invaded
Stage 3b = IVC below diaphragm
Stable 3c = IVC above diaphragm
Stage 4 = Beyond Gerota’s fascia, Ipsilateral adrenal

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16
Q

Polycystic Kidney Disease and RCC

A

APCKD doesn’t itself increase risk of RCC, but it does increase risk of needing dialysis, which increases RCC risk.

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17
Q

Renal lymphoma (4)

A

Can look like anything.
Most commonly bilateral enlarged kidneys with small, low attenuation cortically based solid nodules or masses.
Solitary mass in about 25%.
Lymphoma is most likely renal mass to preserve normal kidney shape

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18
Q

Renal leukaemia (3)

A

Kidney is commonest involved visceral organ in leukaemia..
Typically smooth, enlarged kidneys.
Hypodense lesions are cortically based only, with little medulla involvement if at all

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19
Q

Renal oncocytoma (4)

A

Second commonest benign tumour after AML.
Looks like RCC, but has central scar.
No malignant features (e.g. vessel infiltration).
Cannot be distinguished from RCC on imaging and must be treated as such until proven otherwise. (RCCs can also have the central scar)

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20
Q

Renal oncocytoma - imaging (3)

A

three ways it can appear
1) Solid mass with central scar on CT or MRI
2) Spoke wheel vascular pattern on USS
3) Hotter than surrounding renal cortex on PET

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21
Q

Birt Hogg Dube associations (2)

A

Associated with chromophobe RCC and bilateral oncocytomas

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22
Q

Multilocular cystic nephroma (4)

A

Non-communicating fluid filled locules surrounded by thick fibrous capsule.
Characterised by absence of solid component or necrosis.
Buzzword “protrudes into renal pelvis”
Bimodal occurence (4 year old boys and 40 year old women).

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23
Q

Bosniak cyst classification (5))

A

Class 1: Simple, <15HU, no enhancement.
Class 2: Hyperdense (<3cm). Thin calcifications, thin septations.
Class 2F: Hyperdense (>3cm), minimally thickened calcifications (5% cancer risk)
Class 3: Thick septations, mural nodule, 50% cancer risk
Class 4: Any enhancement (>15HU), 100% chance of cancer

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24
Q

Hyperdense cysts (2)

A

If >70HY and homogenous, it’s benign.
Usually haemorrhagic or proteinaceous cyst

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25
Q

ADPKD (4)

A

Kidneys get progressively larger and lose function, dialysis by 5th decade.
Hyperdense contents and calcified wall frequently seen due to prior haemorrhage.
70% get liver cysts too.
Associated with berry aneurysms.

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26
Q

ARPKD (5)

A

HTN and renal failure.
Liver involvement leads to abnormal bile ducts and fibrosis.
Congenital hepatic fibrosis is always present in ARPKD.
Ratio of liver and kidney disease is inversely related.
US: Kidneys are smoothly enlarged and diffusely echogenic, loss of corticomedullary differentiation.

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27
Q

Uraemic cystic kidney disease (3)

A

40% end stage renal disease pts develop cysts.
Rises with duration of dialysis, affects 90% of dialysis after 5 years.
Increased risk of malignancy with dialysis 3-6x.
Cysts regress after renal transplant

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28
Q

Von-Hippel Lindau (4)

A

AD, multi system disorder. 50-75% renal cysts, 25-50% get RCC
Pancreas: cysts, serous microcystic adenomas, neuroendocrine tumous (islet cell)
Adrenal: Phaeochromocytomas (often multiple).
CNS: Haemangioblastoma of the cerebellum, brainstem and spinal cord

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29
Q

Tuberous sclerosis (6)

A

AD, multisystem disorder.
Hamartomas everywhere (brain, lung, heart, skin, kidneys).
Renal: Bilateral multiple angiomyolipomas, cysts and occasionally RCC in younger people.
Lung - LAM (thin walled cysts and chylothorax)
Cardiac - Rhabdomyosarcoma, typically involves cardiac septum
Brain - Giant Cell Astrocytoma, cortical and subcortical tubers, subependymal nodules

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30
Q

Lithium nephropathy (4)

A

Long term lithium users.
Leads to DI and renal insufficiency.
Kidneys are normal to small volume, multiple tiny cysts, usually 2-5mm.
These are distinguishable from larger cysts associated with acquired uraemia.

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31
Q

Multicystic dysplastic kidney (3)

A

Kids, multiple tiny cysts forming in utero.
No functioning renal tissue.
Contralateral renal tract abnormalities occur 50% of the time

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32
Q

Multicystic dyplastic kidney vs hydronephrosis (2)

A

Hydronephrosis - cystic spaces are seen to communicate.
In difficult cases, renal scintigraphy is useful to demonstrate no excretory function in MCDK

33
Q

Peripelvic cyst vs parapelvic cyst (2)

A

Peripelvic: originates from renal sinus, mimics hydro
Parapelvic: Originates from parenchyma, may compress collecting system

34
Q

T2 Darl renal cyst - DDx (5)

A

Lipid poor AML
- Small percentage of AMLs are lipid poor
- Lipid poor AMLs are associated with TS (30% AMLs are lipid poor)
Haemorrhagic cyst
- Will likely be T1 bright
Papillary RCC
- Clear cells (most common) are T2 Hyperintense.
- Both clear cell and papillary will enhance, but clear cell enhances more avidly (equal to cortex on corticomedullary phase)

35
Q

Pyelonephritis (5)

A

Clinical diagnosis, associated with stones.
Most common organism is E.Coli.
Alternating bands of hypo and hyperattenuation (striated nephrogram).
Wedge shaped areas are related to decreased perfusion.
Perinephric stranding also seen

36
Q

Striated Nephrogram DDx (8)

A

Acute ureteral obstruction
Acute pyelonephritis
Acute renal vein thrombosis
Acutely following renal contusion
Hypotension (bilateral)
Infantile polycystic kidney (bilateral)
Medullary sponge kidney
Radiation nephritis

37
Q

Renal abscess (3)

A

Pyelonephritis may be complicated by abscess.
CT: round or geographic low attenuation collection with enhancing rim.
>3cm and likely need IR drainage.

38
Q

Chronic pyelonephritis (3)

A

Unclear if active chronic infection, arises from multiple recurrent infections, or stable changes from a remote single infection.
Imaging: Renal scarring, atrophy, cortical thinning with hypertrophy of residual normal tissue.
Small deformed kidney, wedge defects and hypertrophied areas.

39
Q

Emphasematous pyelonephritis (3)

A

Life threatening necrotizing infection, characterised by gas formation within or surrounding the kidney.
Almost exclusively in diabetics.
Echogenic foci with dirty shadowing on US.

40
Q

Emphysematous pyelitis (4)

A

Not as bad as emphysematous pyelonephritis.
Gas is localised to the collecting system
More common in women, diabetics, urinary obstruction.
Gas outlining ureters and dilated calices on imaging

41
Q

Pyonephritis (5)

A

Infected or obstructed collecting system (frequently enlarged).
Can be due to stones, tumour, sloughed papilla due to pyelonephritis.
Can harm renal function if untreated.
Fluid-fluid level in collecting system seen on US.
CT can’t reliably tell between hydronephrotsis and pyonephrosis

42
Q

XGP - Xanthogranulomatous pyelonephritis (4)

A

Chronic destructive granulomatous process, basically always seen with staghorn calculus acting as a nidus for recurrent infection.
Can get associated psoas abscess with minimal perirenal infection.
Characteristic bear paw appearance on CT.
Kidney is not functional, Nephrectomy sometimes needed.

43
Q

Papillary necrosis (7)

A

Ischaemic necrosis of the renal papillae, most commonly involves medullary pyramids.
Diabetes is most common cause
Other causes include pyelonephritis (especially kids), sickle cell, TB, analgesia and cirrhosis.
Filling defects can be seen in calyx.
Necrotic cavity in the papillae with linear streaks of contrast inside the calyx (Lobster Claw sign).
50% of Sickle cell patients get papillary necrosis

44
Q

TB (renal) (5)

A

Commonest extrapulmonary site of infection is the urinary tract.
Features of papillary necrosis and parenchymal destruction.
Can get extensive calcification.
End up with shrunken calcified kidney “Putty kidney”.
“Kerr kink” is a sign of renal TB, with scarring leading to a sharp kink in the pelvi-ureteric junction

45
Q

HIV nephropathy (2)

A

Normal sized (or big) kidneys that are echogenic on US.
Loss of renal sinus fat appearance also described (oedema in the fat rather than actual loss of fat)

46
Q

Disseminated PCP

A

in HIV, can result in punctate (mainly cortical) calcifications.

47
Q

Contrast induced nephropathy (3)

A

Allergic reactions are NOT a risk factor for CIN.
Risk factors for CIN include pre-existing renal insufficiency, DM, cardiovascular disease with CHF, dehydration and myeloma.
Hydration via IV with 1/2 normal saline 12hrs before and after contrast administration supposedly decreases CIN in chronic renal insufficiency (true mechanism is diluting creatinine levels)

48
Q

Nephrolithiasis (kidney stones) - types (5)

A

Calcium oxalate (75%),
Struvite - most common in women and associated with UTI
Uric acid - unseen on XR
Cysteine - Rare, associated with congenital disorders of metabolism
Indinavir - Stones in HIV patients, ONLY stones not seen on CT

49
Q

Cortical nephrocalcinosis (3)

A

Sequella of cortical necrosis, can be seen with acute drop in BP.
Starts as hypodense, non rim-enhancing lesion, later develops thin calcifications. Mimic is disseminated PCP

50
Q

Medullary Nephrocalcinosis (4)

A

Hyperechoic renal papilla/pyramids which may or may not shadow.
Multiple causes, commonest either Hyperparathyroid or Medullary sponge kidney.
Others include Lasix use in child, renal tubular acidosis (distal subtype).
RTA and hyperparathyroidism usually cause a more dense calcification than medullary sponge kidney.

51
Q

Medullary sponge kidney (3)

A

Congenital cause of medullary nephrocalcinosis, usually asymmetric.
Underlying mechanism is cystic dilation of collecting tubules. associated with Ehler Danlos.
Also associated with Carolis and Beckwith-Weidman.

52
Q

Page kidney (2)

A

Sequella of long standing compression of the kidney by subcapsular collection (haematoma or seroma).
Classic scenario is post lithotripsy subcapsular haematoma, with follow up scan showing shrunken kidney.

53
Q

Delayed nephrogram vs persistent nephrogram (4)

A

Delayed: One kidney enhances and the other doesn’t.
- Due to pressure on the kidney, either extrinsic from Page kidney, or intrinsic from obstructing stone
Persistent: Hypotension, shock or ATN.
- Dense kidneys on AXR
- Bilateral enhancing kidneys hours after contrast.

54
Q

Renal infarct (4)

A

Best seen on post contrast imaging in cortical phase.
Wedge shaped hypodensity, or entire kidney won’t enhance if renal artery is blocked.
Cortical rim sign: Absent immediately after insult, seen 8hrs to days later. Dual blood supply allows cortex to stay perfused.
Flip flop enhancement: Region of relatively low density/enhancement becomes hyperdense on delayed imaging.

55
Q

Renal vein thrombosis (3)

A

Commonly caused by nephrotic syndrome (adults) or indwelling umbilical vein catheters (neonates). Also caused by dehydration.
Can mimic renal stone (flank pain, enlarged kidney and delayed nephrogram).
Doppler shows reversed arterial diastolic flow and absent venous flow.

56
Q

Renal trauma on CT, next step?

A

Delayed imaging to look for urine leak.

57
Q

Fractured kidney (2)

A

Laceration which extends the full length of the renal parenchyma.
Must connect 2 cortical surfaces, i.e. goes all the way through

58
Q

Shattered kidney (2)

A

More severe form of fractured kidney.
Kidney with 3 or more fragments.

59
Q

High yield renal trauma appearances (3)

A

Wedge shaped hypoattenuation
- Segmental artery injury
Diffuse nonperfusion
- Devascularised kidney
Persistent nephrogram
- Renal vein injury/thrombus

60
Q

Normal renal transplant (3)

A

Should have low resistance flow (always ‘on’).
Upstroke brisk and forward diastolic flow
Normally transplanted into extraperitoneal iliac fossa, anastamosed with iliac vasculature and urinary bladder

61
Q

Significance of RIs in transplant (3)

A

If kidney becomes diseased, the resistance will increase.
Higher the RI, sicker the kidney.
RI should be <0.7, higher is concerning

62
Q

Complications of renal translpant - types (3)

A

Urologic
Vascular
Cancer

63
Q

Urinoma (3)

A

Usually first 2 weeks post op.
Anechoic fluid collection with no septations, rapidly increasing in size.
MAG3 can demonstrate this.

64
Q

Haematoma (4)

A

Common immediately post op.
Usually resolves spontaneously.
Large haematoma can cause hydronephrosis.
Acute haematoma is echogenic, progressively becoming less echogenic (older haematomas become more anechoic and septated)

65
Q

Lymphocele (3)

A

Occur 1-2 months after transplant.
Caused by leakage of lymph from surgical disruption of lymphatics.
Fluid collection medial to transplant, between graft and bladder.

66
Q

Acute rejection/ATN (3)

A

Up to 20% will get some early rejection.
Both ATN and acute rejection tend to occur in first week or so.
Pyramids become more prominent on US, transplant becomes bigger, RI increases.
ATN vs acute rejection: MAG3 (ATN has normal perfusion, rejection doesn’t. both have delayed excretion)

67
Q

Chronic rejection (3)

A

Occurs 1 year post transplant.
Kidney may enlarge, loss of corticomedullary differentiation.
RI increases.

68
Q

Calculous disease

A

Increased risk of stone formation compared to general population

69
Q

Renal artery thrombosis (transplant) (2)

A

Occurs in 1% in first week.
Caysed by kinking, hypercoagulation or hyperacute rejection.

70
Q

Renal artery stenosis (transplant) (5)

A

5-10% of renal transplants, usually at the anastamosis.
Criteria include:
- PSV >200-300cm/s
- PSV ratio >3 (EIA/RA)
- Tardus parvus: measured at main renal artery hilum (not arcuates).
- Anastamotic jetting

71
Q

Renal vein thrombosis (transplant) (3)

A

More common week 2 post op.
Kidney usually swollen.
No flow in renal vein, reversed diastolic flow in renal artery.

72
Q

AVF (transplant) (3)

A

Occur secondary to biopsy in 20%, but most are small and asymptomatic.
Shown with tissue vibration artefact (perivascular, mosaic colour assignment due to tissue vibration), with high arterial velocity and pulsatile venous flow.

73
Q

Pseudoaneurysm (transplant) (3)

A

Occur secondary to biopsy, less common.
Also occur due to graft infection or anastamotic dehiscence.
Classic yin yang colour doppler, or doppler with biphasic flow at neck of pseudoaneurysm

74
Q

Cancer in transplant

A

100x risk of developing cancer due to immunosuppression therapy.

75
Q

RCC (transplant) (2)

A

Increased risk, 90% occur in native kidney.
Unclear aetiology (association with dialysis, immunosuppression or both)

76
Q

Post transplant Lymphoproliferative Disorder (PTLD) (3)

A

Uncommon complication of organ transplant, associated with B-cell proliferation.
Most common in first year of transplant, often involved multiple organs.
Rx: Reduce immunosuppression.

77
Q

Cyclophosphamide (transplant) (2)

A

Significant exposure to cyclophosphamide (less common due to cyclosporin A) increases urothelial cancer.

78
Q

Renal transplant complications (summary) (13)

A

Week 1
- Renal artery thrombosis
- Renal artery stenosis
- Haematoma
- Urinoma
Week 1-4
- Renal vein stenosis
- Lymphocele
Months 1-6
- Drug toxicity
- Lymphocele
- Biopsy related injury (pseudoaneurysm, AVF)
Month 6+
- Chronic rejection
- RCC
- Lymphoma
- PTLD